Kembara Xtra - Medicine - Schizophrenia
A severe and ongoing mental condition marked by delusions, hallucinations, disordered thinking and behavior, cognitive dysfunction, and difficulty judging reality .Major psychiatric condition with a varied course, usually characterized by prodromal, active, and persistent psychotic symptoms as well as problems in cognition, speech, mood, behavior, and perception. Subcategories of schizophrenia such as paranoid, disorganized, catatonic, etc. were dropped from the DSM-5. Central nervous system (CNS) is/are the affected system(s). Incidence 7.7 to 43/100,000 cases per 100,000 Age of onset: typically 30 years, earlier in males (late teens to mid-20s) than in females (early 20s to early 30s), with a smaller peak that occurs in women >45 years. Predominant sex: male-to-female ratio = 1.4:1.0; age of onset: typically 30 years; more subtle changes in cognition and functioning can precede the diagnosis (prodromal period) by several years. Low socioeconomic levels and metropolitan areas have the highest prevalence over the course of a lifetime (1%) (2-fold higher risk). 1.1% of the population over the age of 18; comparable rates worldwide Pathophysiology and Etiology Is the result of a complex interaction between genetic and environmental factors; risk factors for increased occurrence include prenatal infection or hypoxia, winter births, first-generation immigrants, older fathers, drug use, and genetic (velocardiofacial) abnormalities. Perceptual abnormalities, disturbed mental processes, and cognitive deficits are caused by overstimulation of mesolimbic dopamine D2 receptors, prefrontal dopamine deficiency, and aberrant prefrontal glutamate (NMDA) activity. Genetics There is an 8–10% (10-fold) risk of schizophrenia if a first-degree biological relative has it. Prevention Inform every patient about the dangers of marijuana use, but especially those who may be prodromal or have a family history of psychosis. Metabolic syndrome, diabetes mellitus, obesity, and infectious diseases like HIV, hepatitis B, and hepatitis C all occur at higher-than-expected rates. Nicotine dependence (>50%) and substance use disorders. Diagnosis Focus on recognizing a gradual loss in social and functional functioning over a period of around 6 months to distinguish schizophrenia from transient psychotic and schizophreniform disorders. For a minimum of one month, at least two of the following fundamental symptoms must be present: Delusions (constantly held false beliefs) Hallucinations (visual and auditory disturbances) Irregular speech (derailed or confused thought) Extremely chaotic or catatonic behavior (repetitive, hyper- or hypoactive motions) Negative symptoms, including reduced emotional expressiveness, poor speech and cognition, apathy, and lack of social interest clinical assessment There are no outward signs of the illness, but long-term use of neuroleptic medications can cause extrapyramidal symptoms like tardive dyskinesia (repetitive, uncontrollable movements), dystonia (sustained muscle contractions), akathisia (restlessness), parkinsonism (tremor), and stuttering gait. Multiple Diagnoses Schizophreniform disorder (symptom duration: 1 to 6 months) and brief psychotic disorder (symptom duration: 1 month) Disorientation and an altered degree of alertness raise questions about delirium. Psychotic disorder brought on by another medical disease. Alcohol, cocaine, hallucinogens (amphetamines, LSD, phencyclidine), cannabis (including synthetic), bath salts, or prescription drugs including steroids, anticholinergics, and opiates can all cause substance-induced psychosis. - In patients with substance-induced psychosis, schizophrenia develops in about 25% of cases. Cannabis use is linked to transition rates that are the highest. Personality disorders include borderline, schizotypal, schizoid, and paranoid disorders. Posttraumatic stress disorder, autism spectrum disorder, bipolar disorder, major depressive disorders with psychotic characteristics, or catatonia are some examples of mood disorders. Laboratory Results Imaging (MRI), EEG, LP, and laboratory testing may be necessary to rule out other causes and may be utilized when clinical presentation permits, but no tests are currently available to diagnose schizophrenia. Initial Examinations (lab, imaging) The following labs are frequently conducted to exclude a medical cause of psychotic symptoms: - Blood chemistries, complete blood count (CBC), and thyroid-stimulating hormone (TSH) - Vitamin levels (folate, methylmalonic acid/vitamin B12, thiamine, vitamin D, etc) - Blood and urine drug/alcohol screening, as well as urinalysis - Syphilis and HIV testing - Heavy metal exposure: mercury and lead - Ceruloplasmin and, when indicated, urine porphobilinogen - Antinuclear antibody and the rate of erythrocyte sedimentation the hepatitis B and C viruses ● Prior to starting an antipsychotic, the following labs are conducted to check for comorbidities and determine baseline values: - Baseline QTc electrocardiogram (ECG) - TSH, hemoglobin A1C, TSH, CBC, blood chemistries Lipid panel and, if necessary, a pregnancy test Tests in the Future & Special Considerations If taking antipsychotic drugs, routine clinical and laboratory examinations should be performed at least once a year: Weight, waist size, and blood pressure, as well as a CBC, hemoglobin A1C, and lipid panel. ECG, monitoring for QTc prolongation; pregnancy test; prolactin level, if necessary; clinical evaluation of extrapyramidal symptoms using a validated tool such the Abnormal Involuntary Movement Scale (AIMS) Diagnostic procedures and other neuropsychological testing are not typically included in assessments but can be used to determine cognitive functioning and the need for support. Interpretation of Tests No definitive pathologic features, however ventriculomegaly is typically observed on MRI, with whole-brain gray matter loss and selective white matter loss in regions in the medial temporal lobe. MEDICATION FOR TREATMENT First Line There are two categories of antipsychotic drugs: conventional and atypical. An atypical antipsychotic is used as the first line of treatment because to its lower risk of extrapyramidal adverse effects. - Dissimilar (second generation) (Parkinson disease-related psychosis) Risperidone, olanzapine, ziprasidone, aripiprazole, quetiapine, paliperidone, iloperidone, asenapine, lurasidone, clozapine, brexpiprazole, cariprazine, pimavanserin - Common (first generation) Fluphenazine, trifluoperazine, perphenazine, thioridazine, thiothixene, haloperidol, and chlorpromazine The selection of medication is based on the side-effect profile, clinical and subjective response (3). - Atypical sensitivity to extrapyramidal negative effects - Quetiapine and clozapine have the lowest risk of tardive dyskinesia. Aripiprazole, ziprasidone, lurasidone, perphenazine, and brexpiprazole had the lowest chance of developing the metabolic syndrome. Aripiprazole has the lowest risk of QTc prolongation. In patients with a prolonged QT interval, ziprasidone and thioridazine should not be used. Long-acting antipsychotics in injectable form may be utilized for patients with low adherence or a high risk of relapse. - Paliperidone, haloperidol, fluphenazine, risperidone, olanzapine, and aripiprazole Daily range for routine maintenance (The initial dose is frequently lower.) - Chlorpromazine: 200 to 800 mg divided into BID,TID, and QID each day Asenapine: 5 to 10 mg BID (sublingual), once daily patch (FDA authorized in October 2019) - Aripiprazole: 10 to 30 mg/day Lurasidone: 40 to 80 mg/day (with meal) Fluphenazine: 5 to 20 mg/day Haloperidol: 5 to 20 mg/day Paliperidone: 3 to 12 mg/day Olanzapine: 10 to 30 mg/day - 24 mg of perphenazine per day, divided BID/TID 200 to 400 mg BID of quetiapine - Ziprasidone: 20 to 80 mg BID (with lunch) - Risperidone: 2 to 8 mg/day Pimavanserin (for Parkinson disease-related psychosis): 34 mg/day Cariprazine: 1.5 to 6.0 mg/day Brexpiprazole: 2 to 4 mg/day Clozapine: 200 mg BID 300 to 600 mg/day, divided into BID doses, is the usual dosage range. Effective in treating people who are suicidal and the gold standard treatment for schizophrenia Registration with the National Clozapine Registry and weekly to monthly CBC monitoring with differential are required for patients who have a serious risk of agranulocytosis. At larger doses, there is a sizable chance of seizures Myocarditis, DVT, sialorrhea, tachycardia, and weight gain can all be symptoms of SE. ALERT There is a danger of weight gain, metabolic syndrome, and tardive dyskinesia with all antipsychotic medications. Controlling the negative effects of antipsychotics - Dystonic response (particularly of the head and neck): 25 to 50 mg IM diphenhydramine or 1 to 2 mg IM benztropine - Lorazepam 0.5 to 1.0 mg BID or propranolol 20 to 30 mg BID for akathisia (restlessness). Parkinsonism treatment options include amantadine 100 mg daily (up to 300 mg daily), trihexyphenidyl 2 mg BID (up to 15 mg daily), and benztropine 0.5 BID (1 to 4 mg/day). - Valbenazine (80 mg daily), tetrabenazine (25 to 50 mg TID), or deutetrabenazine (6 to 24 mg BID) are medications for tardive dyskinesia. - Neuroleptic malignant syndrome, which includes extrapyramidal symptoms, hyperthermia, and autonomic dysfunction; necessitates hospitalization and supportive care (IVF and stopping the offending neuroleptic). - Metformin and topiramate for metabolic syndromeAll antipsychotics come with a black box warning about an elevated mortality risk in older individuals with dementia. Benzodiazepines are used as adjunctive therapies. First-line for the treatment of catatonia Withdrawal reactions with psychosis or seizures; risk for dependence and cognitive impairment Best when used only briefly; high cumulative exposure to benzodiazepines is associated with a significantly increased risk of death in patients with schizophrenia. - Mood enhancers Valproic acid might be a useful supplement for people who behave violently or agitatedly. Lithium may be a useful supplement for patients who have severe emotional symptoms or suicidal thoughts. - Drugs for depression When added to antipsychotic monotherapy as opposed to adding a second antipsychotic, it is associated with a lower risk of mental hospitalization, which is helpful if concomitant depression and/or anxiety are present. Referral: Multidisciplinary care from a primary care clinician and a psychiatrist is advised in cases of suicidality, co-occurring substance use disorder, trouble engaging, or poor self-care. Families frequently gain from being directed to family advocacy groups like NAMI. Further Treatments • Psychoeducational and psychotherapeutic interventions for the patient and family, including targeted therapies to lessen the severity of psychotic symptoms, improve social functioning, and lower the risk of symptom exacerbation. Cognitive remediation is a new approach for cognitive retraining and psychosocial recovery. Vocational support programs have shown success in getting people back to work. Cognitive-behavioral therapy has been shown to be effective for certain symptoms of schizophrenia. Negative symptoms typically respond better to these nonpharmacologic interventions than they do to medications. Surgical Techniques Patients exhibiting catatonic symptoms, severe depression, aggressiveness, or suicidal ideation should be given electroconvulsive therapy (ECT) consideration. Admission The decision to enter is made based on the likelihood of danger to oneself or others, as well as the inability to take care of oneself. Monitoring is based on the evaluation of symptoms (including safety and psychotic symptoms), looking for the emergence of comorbidities, medication side effects, and prevention of complications. Long-term symptom management and rehabilitation depend on engagement in ongoing pharmacologic and psychosocial treatment. The risk of metabolic side effects such diabetes, hypercholesterolemia, and weight gain is increased when using diet antipsychotics. Prognosis: Although rare, there are reported cases of total remission and refractory sickness. The typical history is one of remissions and exacerbations. Positive symptoms are easier to manage with antipsychotics than negative ones, which are sometimes the most challenging. 20% of people attempt suicide, and 5-6% of those who do so do so fatally. Complications Combative conduct toward others (Note that only 5% of crimes are committed by people with mental illness, including psychosis, and the mentally ill are more likely to be victims of violence.) Medication side effects (tardive dyskinesia, orthostatic hypotension, QTc prolongation, metabolic syndrome). Substance use disorders that coexist
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Kembara Xtra - Medicine - Scleritis Scleritis is an inflammatory, painful condition that affects the sclera, the outer layer of the eye. - Divided into diffuse, nodular, or necrotizing lesions that are anterior or posterior. - Frequently linked to systemic problems - Possibly a hazard to vision Episcleritis, in contrast, is a mildly uncomfortable inflammation of the superficial episclera that self-limits. ocular system(s) affected Epidemiology With a range of 12 to 96, the average age is 54. Female is more prevalent than male (1.6:1) Incidence 6 incidents per 100,000 people in the general population, according to estimates Prevalence In approximately 94% of cases, anterior scleritis (1) - Diffuse anterior scleritis, most prevalent (75%). 6% of the group still has posterior scleritis. Pathophysiology and Etiology Frequently accompanied by a systemic condition – Most frequently accompanied by rheumatoid arthritis – Scleritis is the outward sign of a systemic disorder in 38% of cases. - The strongest correlation between systemic illness and necrotizing scleritis is observed. Other causes are - Type of scleritis affects the proposed pathogenesis. The main cause of necrotizing scleritis is probably linked to the action of matrix metalloproteinases. - Scleritis caused by medication has been documented in patients receiving bisphosphonate therapy. - Surgically induced necrotizing scleritis is extremely uncommon and develops after several operations. - The most frequent cause of infectious scleritis in poorly managed diabetic individuals is Pseudomonas aeruginosa. This condition most frequently follows surgical trauma. Risk Elements Most at risk are people with autoimmune diseases. Rheumatoid arthritis is the most prevalent associated condition, followed by Sjögren syndrome, granulomatosis with polyangiitis, HLA-B27-associated ankylosing spondylitis, Behçet disease, juvenile idiopathic arthritis, Cogan disease, relapsing polychondritis, polyarteritis nodosa, sarcoidosis, inflammatory bowel disease, herpes zo Sclera that is red and inflamed is the diagnosis. - About 40% of cases might be bilateral. The pain can be described as persistent, deep, boring, or pulsating. It may refer to the eyebrow, temple, or jaw. It may cause the patient to wake up in the early morning hours. Other symptoms include photophobia and tears. Necrotizing scleritis is most frequently linked to extremely painful symptoms. Clinical evaluation Sclera should be visually inspected in all directions. - A bluish tint may indicate sclera thinning. - Check for injection volume and tissue thinning. Verify your visual acuity. - two or more points of visual acuity loss A patient's Snellen lines appear in 16% of cases. Slit-lamp examination reveals episcleritis: anterior displacement of the superficial vascular plexuses and blanches in response to phenylephrine. - Scleritis: In patients with episcleritis, the distinctive blue or violet color is missing, and the deep episcleral plexus exhibits the greatest vascular congestion. To rule out posterior involvement, perform a dilated fundus exam. A thorough physical examination should be conducted to check for any linked disorders, paying special attention to the skin, joints, heart, and lungs. Conjunctivitis, episcleritis, anterior uveitis, posterior uveitis, blepharitis, and ocular rosacea are among the differential diagnoses. Laboratory Results Standard diagnostic procedures to rule out systemic disease: CBC, serum chemistry, urinalysis, ESR, and/or C-reactive protein, blood, and urine cultures Particular diagnostics for systemic illnesses that are underlying: The following tests may help with the diagnosis: rheumatoid factor, anticyclic citrullinated peptide antibodies, ACE level, HLA-B27, antineutrophil cytoplasmic antibodies, PPD or QuantiFERON-TB level, fluorescence treponemal antibody absorption (FTA-ABS), rapid plasma regain (RPR), Lyme titers, and antinuclear antibody. If a specific systemic ailment is suspected, additional imaging tests, such as a chest x-ray, sacroiliac joint films, or colonoscopy, may be helpful. B-scan US for posterior scleritis detection. Check the sclera's thickness as well as the presence of T-sign (fluid in Tenon's space at the sclera's junction with the optic nerve). An MRI/CT scan may be able to identify ocular illness and offer extra diagnostic value. ● Different scleritis subtypes are linked to various presentations and distinctive findings: - Diffuse anterior scleritis: extensive swelling Necrotizing anterior scleritis: "with inflammation": Sclera turns translucent. Nodular anterior scleritis: immobile, inflammatory nodule. Scleromalacia perforans without inflammation is painless and frequently linked to rheumatoid arthritis. Posterior scleritis is linked to troubles with the retina and choriocapillaris, as well as possible orbital tissue enlargement. Unless the diagnosis is still unclear following the aforementioned examinations, diagnostic procedures or further biopsies are not usually necessary. If you think the cause is infectious, culture it. Management If scleral thinning, eye protection such as glasses should be used to prevent perforation, and the condition should be managed by a qualified eye care specialist. First-line treatments for noninfectious scleritis include oral NSAID medication; examples are ibuprofen 600 to 800 mg PO TID-QID or indomethacin 50 mg PO TID, assuming there are no contraindications (5).[B] Prednisone 40 to 60 mg PO QD or 1 mg/kg/day, taper over 4 to 6 weeks. Systemic steroids (initial if necrotizing scleritis and preferred IV if eyesight threatening, else use if NSAIDs fail). If you suspect an infectious cause, exercise caution. - As steroid-sparing medications, antimetabolites like methotrexate, azathioprine, mycophenolate mofetil, cyclophosphamide, and cyclosporine may be utilized. If steroids cannot be weaned below 10 mg PO QD, they are usually advised. Secondary treatments If a patient has tried and failed with antimetabolites or calcineurin inhibitors, or if they are not a candidate, they can be treated with immunomodulatory drugs such infliximab, rituximab, and adalimumab. Due to their better treatment outcomes and possibly paradoxical effects on ocular inflammation, these medications are preferred to etanercept. Adjunct therapy considerations include: Topical steroids (prednisolone acetate 1% or difluprednate 0.05% when administered under ophthalmologist supervision), subconjunctival triamcinolone acetonide injections (40 mg/mL only for non-necrotizing), and increased risks of cataract and globe perforation. Necrotizing anterior and posterior scleritis: In addition to systemic steroids, immunosuppressive medication may be necessary. - In order to prevent problems, treat quickly. Patch grafting may be required to maintain the integrity of the globe. About 18% of infectious cases are resolved with antibiotic therapy, but the remainder instances frequently necessitate surgical intervention, such as débridement. All patients with scleritis should be treated by an ophthalmologist who is knowledgeable about this ailment. Referral to rheumatology for concurrent systemic disease is beneficial for long-term success. Further Treatments Active scleritis may benefit from immunosuppressive medications used for autoimmune and collagen vascular diseases. Operations Scleral biopsy may be necessary in rare circumstances to confirm an infection or another etiology. Scleral grafting is necessary for ocular perforation. Take Action Avoid using contact lenses; only do so if the cornea is involved, which is uncommon. patient observation An ophthalmologist should monitor patients with inflammation that is still active extremely attentively in order to gauge how well their treatment is working. The use of medication necessitates rigorous monitoring for side effects. Scleritis has an indolent, persistent, and frequently progressive prognosis. The best prognosis for anterior scleritis is diffuse, while the worst prognosis is necrotizing anterior scleritis. There may be recurrent flare-ups of inflammation. Scleromalacia perforans poses the greatest threat to the integrity of the earth. Complications include vision loss, anterior uveitis, ocular HTN, and peripheral keratitis. Steroid therapy can also cause cataract and glaucoma. Ocular perforation can progress to a dangerous level. Kembara Xtra - Medicine - Scarlet Fever An illness (mostly affecting children) brought on by group A -hemolytic Streptococcus pyogenes (GAS), which produces erythrogenic toxin, and characterized by fever, pharyngitis, and rash Rash typically appears 24 to 48 hours after the first symptoms appear and spreads quickly throughout the body, starting in the groin, trunk, and axillae with strawberry tongue and circumoral pallor. Rash clears at the end of the first week and is followed by several weeks of desquamation. Rash is not dangerous but is a marker for GAS infection with suppurative and nonsuppurative symptoms. Head, eyes, ears, nose, throat, skin/exocrine, and afflicted system(s) Similar word(s): scarlatina Incidence In wealthy nations, 4- 10% of adults and 15% of school-age children experience GAS pharyngitis each year. Because of maternal antitoxin antibodies, scarlet fever in infants is uncommon. Males predominate in the United States among individuals over 12 years old due to high rates (>80%) of lifetime protective antibodies to erythrogenic toxins. Peak age is between 4 and 8 years. Prevalence 10% of children with streptococcal pharyngitis develop scarlet fever; GAS accounts for 15–30% of cases of pharyngitis in children and 5–15% in adults. Pathophysiology and Etiology It need the generation of erythrogenic toxin for scarlet fever to occur. There are three different categories of toxins: A, B, and C. Toxins injure capillaries (resulting in rash) and function as superantigens, inducing the release of cytokines. The primary site of streptococcal infection is typically within the tonsils, but scarlet fever can also occur with infection of the skin, surgical wounds, or uterus (puerperal scarlet fever). Antibodies against toxins reduce formation of rash but do not protect against underlying illness. Risk factors include a seasonal increase from winter to early spring, a higher prevalence in school-aged children, contact with infected people, and crowded living situations (such as those associated with a lower socioeconomic position, barracks, child care centers, and schools). Prevention Spread through contact with saliva, nasal secretions, and airborne respiratory droplets Although they are uncommon, foodborne outbreaks have been reported. Asymptomatic contacts do not require prophylaxis or cultures. The necessary laboratory tests should be performed on symptomatic contacts of a child with a confirmed GAS infection who have recent or present clinical signs of a GAS infection. If the tests are positive, the contacts should be treated. Children should wait until they are afebrile and have had 24 hours of antibiotic therapy before going back to school or daycare. Associated Conditions:Glomerulonephritis, rheumatic fever, impetigo, pharyngitis, and Prodrome a day or two Fever (>38°C [100.4°F]), sore throat, headache, myalgias, malaise, and fever Vomiting and stomach pain (which could mimic an acute abdomen) Rash is a scarlatiniform erythematous punctate eruption. Viral infections are more frequently linked to cough, conjunctivitis, hoarseness, diarrhea, coryza, oral ulceration, and rhinorrhea. clinical assessment Oral examination: beefy red tonsils and throat, with or without exudate; petechiae on the palate; and a white coating on the tongue (appearing between days 1 and 2). By days 4 to 5, this sheds, leaving a red strawberry tongue that is glossy, erythematous, and has noticeable papillae. Exanthem (appearing in one to five days) - Blurs when squeezed; scarlet, nonconfluent, 1 to 2 mm papules with widespread erythema "Sunburn with goose pimples" is an orange-red, punctate skin eruption with a sandpaper-like texture. Coarse "sand paper" rash that first appears in the groin, upper trunk, and axillae before moving to the extremities is prevalent in skin folds and flexural surfaces (such as the axillae, groin, and buttocks), sparing the palms and soles. - Pale lips, flushed face, and circumoral halo Pastia lines: transverse red streaks in the skin folds of the abdomen, antecubital space, and axillae. Desquamation. After 7 to 10 days, desquamation starts on the face and spreads over the trunk to the hands and feet. In severe cases, small vesicular lesions (miliary sudamina). Differential diagnosis includes: infectious mononucleosis; mycoplasma pneumonia; secondary syphilis; toxic shock syndrome; staphylococcal scalded-skin syndrome; Kawasaki disease; acute systemic lupus erythematosus; juvenile arthritis; drug hypersensitivity; severe sunburn. Viral exanthem includes: measles, rubella, roseola, and erythema infectiosum (the fifth disease). Laboratory Results The clinical features of streptococcal and nonstreptococcal pharyngitis overlap too much for a precise diagnosis to be made on those grounds alone. Even patients with all of the clinical signs and symptoms, particularly in children, only have streptococcal pharyngitis 35 to 50 percent of the time. Use the outcomes of quick tests based on polymerase chain reaction (PCR) or rapid antigen detection testing (RADT). Modifications to the Centor clinical decision rule - 1 point for not coughing - Anterior cervical nodes 1 point are swollen and painful. - The temperature was 100.4°F (38°C). 1 point - One point for tonsillar exudate or edema - From 3 to 14 years of age, 1 point Ages between 15 and 44: 0 points; ages over 45: 1 points Cumulative score - 0: No additional testing or antibiotics are recommended due to the low risk of GAS pharyngitis (1-2.5%). Risk of GAS pharyngitis is 1: 5-10%; no additional testing or antibiotics are recommended; alternative tests include throat cultures and RADT; if positive, treat. Risk of GAS pharyngitis in groups of two: 11–17%; perform throat cultures or RADT; treat if positive; and 28–35%; perform throat cultures or RADT; treat if positive. - 4+: Risk of GAS pharyngitis is 51-53%; think about empiric antibiotic treatment. Patients who exhibit symptoms that point to a viral cause (such as cough, coryza, diarrhea, conjunctivitis, rhinorrhea, hoarseness, or oral ulcers) should not have testing for GAS pharyngitis done. Initial examinations (lab, imaging) RADT: if positive, a diagnostic test with sensitivity similar to culture and 95% specificity. throat culture should be used to confirm a negative RADT in children (adults do not need this step). Confirmatory culture is not necessary for positive RADT. PCR: 100% sensitive, 94.1% specific, 84.1% positive predictive value, and 100% negative predictive value when positive. Confirmatory culture is not necessary for positive PCR. The gold standard for diagnosing streptococcal infection is throat culture (99% specific, 90-97% sensitive; 5-10% of healthy people are carriers). Serologic tests (antihyaluronidase, antistreptolysin O titer, and streptozyme testing): Confirm recent GAS infection; neither useful or advised for acute illness diagnosis Gram stain: chains of gram-positive cocci Elevated WBC count (12,000–16,000/mm3) and eosinophilia later (second week) may be seen on CBC. Follow-up throat cultures or RADT/PCR are not typically advised after treatment. Asymptomatic household members of patients with acute streptococcal pharyngitis should not typically undergo diagnostic tests or empiric treatment. Tests in the Future & Special Considerations Within 5 days of symptoms, antibiotics can delay or abolish the antistreptolysin O response. Recent antibiotic medication may have an impact on culture results. Interpretation of Tests Skin lesions show a typical inflammatory response, particularly hyperemia, edema, and infiltration of polymorphonuclear cells. Management Supportive therapy, including the use of analgesic/antipyretic medications like acetaminophen or NSAIDs for moderate to severe symptoms or to reduce fever. Topical anesthetics and pharmaceutical throat lozenges are two options for treating symptoms. First Line of Medicine The main goal of treating GAS is to lower the chance of developing acute rheumatic fever. Early intervention reduces the amount of time that symptoms last by one to two days and shortens the contagious period. The best treatment for GAS pharyngitis is penicillin because of its well-established effectiveness, safety, specificity, and affordability. Penicillin (PO; penicillin V; etc.) for 10 days - 250 mg PO BID or TID for individuals weighing under 27 kg (60 lb); 250 mg QID or 500 mg BID for individuals weighing over 27 kg (60 lb) Adults and adolescents - Use penicillin G benzathine: single IM dose 600,000 U for those under 27 kg (60 lb); 1.2 mU for those over 27 kg if compliance is doubtful. Amoxicillin (PO) 25 mg/kg twice day for 10 days, or 50 mg/kg once daily (maximum dose 1,000 mg) (use only for conclusive GAS as it might cause rash with other viral illnesses). Penicillin allergy is a contraindication. Amoxicillin works similarly to penicillin but is more tolerable to youngsters. Patients with penicillin allergy (anaphylaxis) should avoid taking this medication. Next Line for those with penicillin allergies Type IV penicillin hypersensitivity Cephalosporins used orally First-generation cephalosporins are less expensive but many are effective: Cefadroxil 30 mg/kg once daily; maximum 1,000 mg for 10 days Cephalexin 20 mg/kg dose twice daily for 10 days; maximum 500 mg every 12 hours Type I hypersensitivity to penicillin: 12 mg/kg/day (maximum 500 mg) for 5 days of azithromycin (Zithromax, Z pack). - For clarithromycin (Biaxin), adults should take 250 mg BID for 10 days; children older than 6 months should take 7.5 mg/kg BID. - For 10 days, provide clindamycin 7 mg/kg (max 300 mg/dose) TID.Sulfonamides and tetracyclines shouldn't be utilized. ALERT Due to the possibility of Reye syndrome, youngsters should not take aspirin. Referral Retropharyngeal abscess with peritonsillar abscess; shock symptoms including hypotension, DIC, heart, hepatic, and renal failure Surgery Tonsillectomy is advised in cases of recurrent pharyngitis (6 positive strep cultures in a year). Even while children who have had tonsillectomies are less likely to contract infections, such as streptococcal pharyngitis (often known as "strep throat"), the operation does lessen their likelihood. Follow-Up If there are no symptoms, a follow-up throat culture is not required. Patient Monitoring Treatment failures usually result from: Poor adherence to approved antibiotic medication -Lactamase oral flora hydrolyzing penicillin GAS carrier status and concurrent viral rash (needs no treatment) Streptococci can remain on unrinsed toothbrushes and orthodontic appliances for up to 15 days, resulting in recurrent exposure to carriers in the family. Resolve recurring GAS pharyngitis with the same medication, a different oral medication, or intramuscular penicillin G. No specific diet required Modification of Lifestyle The risk of rheumatic fever is not increased by delaying therapy while waiting for the findings of the culture. Finish the antibiotic course completely. Children shouldn't go back to school or daycare until they've gotten antibiotic therapy for at least 24 hours. Spreads from person to person. Wash your hands frequently, and avoid sharing utensils. Treatment reduces symptoms by 12 to 24 hours, however recurrent attacks (caused by other erythrogenic toxins) are possible. Complications Suppurative, sinusitis, otitis media/mastoiditis, cervical lymphadenitis, peritonsillar abscess/retropharyngeal abscess, and pneumonia are among the complications. Meningitis, brain abscess, osteomyelitis, septic arthritis, endocarditis, cerebral venous sinus thrombosis, and necrotizing fasciitis are a few examples of bacterialemia with metastatic infectious foci. Nonsuppurative - Rheumatic Fever: When treatment is started up to 10 days after the onset of acute GAS infection, it prevents rheumatic fever. - Glomerulonephritis: caused by a Streptococcus nephritogenic strain; prevention, even after proper GAS treatment, is less definite. Fever, hypotension, DIC, and heart, liver, and/or renal damage as a result of various toxin-mediated sequelae are all symptoms of the streptococcal toxic shock syndrome. Poststreptococcal reactive arthritis is an aseptic inflammation of one or more joints that occurs after a pharyngeal streptococcal infection with a symptom-free period and usually without cardiac involvement. Cellulitis - Transverse grooves in nail plates and hair loss (telogen effluvium) may appear weeks to months later - Pediatric autoimmune neuropsychiatric disease associated with GAS (PANDAS). There is a certain group of kids whose obsessive-compulsive disorder (OCD) or tic disorders are made worse by GAS infection. Kembara Xtra. -Medicine - Scabies A contagious skin parasite infection brought on by the Sarcoptes scabiei, var. hominis mite .Skin/exocrine system(s) impacted; typically a clinical diagnosis based on medical history and physical examination Incidence In a retrospective analysis of the nationally representative National Emergency Department Sample for 2013 to 2015, male children from lower income quartiles were more likely to visit the ED, while older male patients, insured by Medicare, from the highest income quartile in the Midwest/West were most likely to be admitted to the hospital. Prevalence Worldwide prevalence varies greatly, although it is more prevalent in places with few resources. More common in crowded places and emerging nations, especially those with tropical climates .Added to the list of neglected tropical illnesses maintained by the World Health Organization in 2017 Pathophysiology and Etiology Hominis variant of S. scabiei .The female mite lays eggs in burrows in the stratum corneum and epidermis. The itching is brought on by a delayed type IV hypersensitivity reaction to the mite saliva, eggs, or excrement. The mite is an obligate human parasite that is primarily transmitted by prolonged human-to-human direct skin contact. Risk Elements Long-term skin-to-skin contact, including that caused by sexual activity, crowding, and nosocomial infections; inadequate nutrition, homelessness, and poverty; and hot, tropical climates .Immunocompromised individuals, notably those with HIV/AIDS, are at increased risk of developing severe (crusted/Norwegian) scabies. Seasonal variation: Incidence may be higher in the winter than in the summer (owing to overcrowding). Prevention By quickly treating and eliminating the fomites, you can prevent outbreaks. Generalized itching is frequently acute and is worse at night. Determine any possible interaction with affected people. For the first 3 to 4 weeks (until sensitivity sets in), the initial/primary infection is normally asymptomatic. The symptoms of a subsequent reinfection usually appear 1 to 3 days following the initial infection. Clinical evaluation Lesions (inflammatory, erythematous, pruritic papules) are most frequently found in the finger webs, flexor surfaces of the wrists, elbows, axillae, buttocks, genitalia, feet, and ankles; in adults, they frequently spare the head and neck. Burrows are thin, curvy lines in the upper epidermis that range in length from 1 to 10 mm, and they are a pathognomic sign. Pustules (if secondary infected) and pruritic papular or nodular lesions in covered areas (buttocks, groin, axillae) as a result of an increased hypersensitivity reaction . Crusted scabies, also known as Norwegian scabies, is a psoriasiform dermatosis caused by an extreme mite infestation (particularly prevalent in immunosuppressed patients). Aspects of Geriatrics In spite of having fewer cutaneous lesions, older people frequently itch more intensely and are more likely to experience widespread infestations, which may be caused by a loss in cell-mediated immunity. Those who are bedridden might experience back involvement. Child Safety Considerations Vesicles, papules, and pustules are frequently found in infants and young children, and they typically include a larger area, such as the hands, palms, feet, soles, body folds, and head (rarely in adults). Differential diagnosis: Papular urticaria, Pediculosis corporis, Dermatitis herpetiformis, Eczema, Folliculitis/impetigo, Psoriasis (crusted scabies), Pyoderma, Seborrheic dermatitis, Syphilis, Tinea corporis Based on 2018 IACS (International Alliance Control for Scabies) findings Criteria for the Scabies Diagnosis: - Scabies diagnosis that has been verified: based on microscopic detection of mites, eggs, or fecal pellets (scybala) OR dermoscopy-based mite visibility. - To diagnose clinical scabies, look for burrows, or look for characteristic lesions in a typical distribution with two historical features: itching and known infected contact. - Typical lesions in a typical distribution with one history of itching or a known infected contact, OR atypical lesions in an atypical distribution with two history features of itching and a known infectious contact, are diagnostic of suspected scabies. The absence of mites does not exclude scabies. CBC is rarely required but may demonstrate eosinophilia on initial tests (lab, imaging). Other/Diagnostic Procedures Look for typical burrows in finger webs, on the flexor side of the wrists, and on the penis while using dermoscopy to examine the skin. - The mite, often known as the "delta wing sign," can be found as a black spot at the end of the burrow. Apply a drop of mineral oil to a nonexcoriated lesion or burrow when scraping the skin. - Use a surgical blade to scrape the lesion . - Use a microscope to check scrapings for mites, eggs, egg casings, or excrement. - Scraping beneath fingernails might be beneficial. - If mites are not discovered through scraping, a biopsy may find mites, eggs, or feces. It is not advised to use potassium hydroxide (KOH) for wet mounting since it can disintegrate mite pellets. Test for burrows with India ink or gentian violet on a rashy region if there are no evident burrows. Use alcohol to remove the ink. Burrows should continue to stain and become more noticeable. Then, as previously mentioned, add mineral oil, scrape, and observe under a microscope. Interpretation of Tests Even though it is rarely done, a skin biopsy of a nodule will show bits of the mite in the corneal layer. Treat all intimate relationships respectfully, especially those with close friends and family. Handle objects that come in contact with skin. All clothing, blankets, and towels should be washed in hot (60°C) water and dried in a hot dryer. Items belonging to the individual that cannot be washed should be kept in a plastic bag for at least seven days. ● With the right care, itching and dermatitis can last up to 4 weeks, however oral antihistamines and/or topical/oral corticosteroids can help. Patients need to be informed that this is probably not a sign that their treatment is failing. However, if symptoms linger for more than 4 weeks after treatment, more testing may be necessary to rule out a different diagnosis, a failure of the first course of treatment, or side effects from the course of treatment. First Line of Medicine The first-line treatment of choice is typically 5% permethrin lotion (Elimite). - Apply cream from the neck to the soles of the feet after taking a bath or shower, paying special attention to the regions that are most affected. After 8 to 14 hours, rinse off the cream. - It is advised to repeat the course of treatment one to two weeks later. - The typical adult dose is 30 g per treatment. Itching, stinging, erythema, and burning (limited absorption) are some of the side effects. Stromectol (ivermectin) is not FDA-approved for treating scabies. The CDC recommends a 200g/kg PO single dose that can be given up to twice in two weeks. It has been demonstrated that failure of a second dosage of ivermectin is a predictor of unsuccessful therapy (4). - To increase bioavailability and increase penetration into the epidermis, take with meals. For HIV-positive patients, larger doses or a combination with topical scabicide may be necessary. - Headaches and nausea may be side effects. There are no very significant differences between permethrin and ivermectin in terms of their associations with high clearance rates in the treatment of scabies. Depending on the specific circumstance, choosing between permethrin or ivermectin can be based on availability, suitability, and associated cost. Permethrin must be applied more frequently (every two to three days for one to two weeks) in cases of crusted scabies, along with repeated doses of oral ivermectin on days 1, 2, 8, and 15. Ivermectin doses may need to be increased in severe instances on days 22 and 29. Child Safety Considerations Infants older than two months old can use permethrin. The cream should be applied to the head, neck, and full body of children under the age of five. Children under the age of five and those weighing less than 15 kg should not receive PO ivermectin. Next Line Crotamiton (Eurax) 10% cream can be applied to newborns older than three months. Apply from the neck down for 24 hours, wash it off, reapply for another 24 to 48 hours, and then completely wash it off. Scabies nodules: Apply to nodules for 24 hours, wash off, reapply for another 24 hours, and then completely wash off. Petrolatum with precipitated sulfur 2-10% - not FDA-approved for scabies - Apply all over the body from the neck down for 24 hours, rinse with water in the shower, and then repeat for an additional 2 days (a total of 3 days). Although smelly and filthy, it is believed to be safer than lindane, particularly for newborns under the age of six months, and safer than permethrin for infants under the age of two months. Apply a thin layer of lindane (-benzene hexachloride, Kwell) 1% lotion to all skin surfaces starting at the neck and washing it off six to eight hours later. - Although it is advised to use two applications spaced one week apart, toxicity risk may increase. - For an adult, 2 oz is usually sufficient. - Neurotoxicity (seizures, muscular spasms), aplastic anemia, and other side effects Uncontrolled seizure disorder and premature newborns are contraindicated. - Caution: Avoid using on skin that has been excoriated, in patients who are immunocompromised, in situations where seizures may be more likely to occur, or when taking drugs that lower the seizure threshold. - Possible interactions include using it concurrently with drugs that lower the seizure threshold. - There have been some reports of scabies that is lindane-resistant. Permethrin does work on these conditions. Use Lindane only if all other options have failed; FDA black box warning of serious brain harm. Child Safety Considerations When administering lindane to individuals who weigh less than 50 kg, the FDA advises caution. It is not advised for infants, and premature infants should not use it. Crotamiton or a sulfur treatment should be used to treat infants under two months old. Pregnant women's issues Permethrin is considered compatible with lactation, however if taken during breastfeeding, the infant should be bottle-fed until the cream has been completely removed. Permethrin is pregnancy Category B, while lindane, ivermectin, and crotamiton are Category C. Referral If unable to confirm diagnosis and/or resistant to repeated treatments, think about referring to dermatologist. Further Treatment Keratolytics may be needed to increase permethrin penetration in cases with crusted scabies. If nodular scabies persists for a number of weeks after treatment, intralesional steroids may be necessary for complete cure. Benzyl benzoate lotion, which is extensively used in underdeveloped nations but is unavailable in the United States, is not FDA-approved for treating scabies. - Adult dosage is 25–28%; for children and babies, dilute to 12.5% and 6.25%, respectively. - Apply lotion from the neck to the soles of the feet after a bath for 24 hours. Topical ivermectin 1% lotion is not FDA-approved for treating scabies (investigative, intermediate level of assurance). - Apply to the afflicted areas, then rinse after eight hours. Alternative Therapies An alternate option for treating scabies that is secure, efficient, and typically well accepted is tea tree oil (TTO), which is derived from the plant Melaleuca alternifolia. In vitro scabicidal effectiveness of 5% TTO has been demonstrated. A low incidence of negative effects (irritant or localized reactions to the oil) is often linked to topical administration of TTO (6). - TTO concentrations less than 20% can be used to prevent the majority of irritating skin responses. Patient Follow-Up Monitoring If the patient's rash or itching doesn't go away, only recheck them every week. Scrape fresh sores, and if mites or products are discovered, withdraw. Lifestyle Modification Patients should receive instructions on how to use the drug correctly and be warned against overusing it when applying it to the skin. The prognosis is that lesions will start to heal in one to two days, but eczema and itching may linger for up to four weeks after therapy. After treatment, complications including eczema and nodules (nodular scabies) may linger for weeks to months. Postscabetic pruritus, insomnia brought on by pruritus, and pyoderma Secondary bacterial infection (particularly prevalent in underdeveloped nations). Sepsis, poststreptococcal glomerulonephritis, and rheumatic heart disease can result from impetigo brought on by Group A Streptococci and Staphylococcus aureus. Social isolation. Kembara Xtra - Medicine - Sarcoidosis Sarcoidosis is a multisystem, noninfectious, granulomatous disease that primarily affects young and middle-aged individuals.Frequently has lung infiltrates, eye or cutaneous lesions, as well as bilateral hilar adenopathy. -Abnormal chest x-rays (CXRs) are used to diagnose it in about 50% of instances in people who have no symptoms. Any organ could be affected. Mainly the pulmonary system, but also the cardiovascular, gastrointestinal, hematologic, endocrine, renal, neurologic, dermatologic, ophthalmologic, and musculoskeletal systems are impacted. Synonym(s): Besnier-Boeck disease; Boeck sarcoid; Scheuermann disease; Löfgren syndrome (erythema nodosum [EN], hilar adenopathy, fever, arthralgias); Heerfordt syndrome (uveitis, parotid hypertrophy, facial palsy, fever); Epidemiology Estimated incidence is 6 per 100 person-years. Estimated prevalence of 10 to 20/100,000 people, with a female incidence rate of 11/100,000 per year. Usually affects younger people, with men and women experiencing the peak incidence between the ages of 40 and 59 and 50 to 69 respectively. Unusual in children Pathophysiology and Etiology Despite intensive research, the cause is still unknown. The initial lung lesion is CD4+ T-cell alveolitis, which results in noncaseating granulomata and may go away or may undergo fibrosis. This lesion is thought to be caused by an excessive cell-mediated immune response to unknown antigen(s). "Immune paradox" occurs when other organs are anergic but the affected organs display a strong immune response. Reports of familial clustering have been linked genetically to a region of the MHC on the short arm of chromosome 6. Despite being widespread, it is more common in Scandinavians, Japanese, Black Americans, and women. Between 5 to 40 cases per 100,000 people in Northern Europe. 35 instances per 100,000 Black Americans, compared to 11 cases per 100,000 Caucasian Americans Risk Elements The exact pathogenesis and etiology are yet unknown. Diagnosis All individuals with probable sarcoidosis should have a thorough examination. Patients may not have any symptoms in the past. Patients may complain in general terms about the following: - An ineffective cough or breathlessness - A fever or nocturnal sweats - Losing weight - General weariness - Headaches - Palpitations - Eye pain Skin lesions, polyarthritis, encephalopathy, seizures, and (rarely) hydrocephalus - Systemic symptoms are more common in patients over 70 years old. Clinical evaluation The majority of patients get a routine physical examination. The lungs may show wheezing or tiny interstitial crackles. 30% of patients experience extrapulmonary symptoms, which may include: - Uveitis or further eye conditions: cataracts, glaucoma, papilledema, lacrimal gland hypertrophy, conjunctival nodules, - Palsies of the cranial nerve - Arrhythmias - Hepatosplenomegaly - Polyarthritis - Rashes - Salivary gland edema or lymphadenopathy - Maculopapular of nares, eyelids, forehead, base of neck near hairline, and past trauma sites Plaques (lupus pernio) on the nose, cheeks, chin, and ears; waxy nodular of the face, trunk, and extensor surfaces of the extremities EN (a part of the Löfgren syndrome) Differential diagnosis Infectious granulomatous conditions like TB and fungi Pneumonitis with hypersensitivity, lymphoma, or other cancers The erylliosis Laboratory Results There is no conclusive test for diagnosis, although the following factors point to one: Radiographic and clinical symptoms -excluding alternate diagnosis. Identification of noncaseating granulomas by histopathology Initial examinations (lab, imaging) Hypergammaglobulinemia, eosinophilia, and leukopenia on the CBC . Hepatic involvement with abnormal liver function and elevated alkaline phosphatase. Up to 10% of patients experience hypercalciuria; hypercalcemia is less common. Serum ACE is high in more than 75% of cases, however it's neither diagnostic nor disqualifying - Drug use can affect test results: Prednisone will normalize the gallium scan and reduce serum ACE. ACE inhibitors reduce the level of ACE in the serum. - Lab results may be affected by disorders: Diabetes, TB, hyperthyroidism, and various malignancies can also raise the serum ACE level. Granulomas and hilar adenopathy may be seen on a CXR or CT scan. Using Scadding classification, CXRs are staged. Normal is stage 0, bilateral hilar adenopathy is stage 1, and parenchymal infiltrates, mainly in the upper lobes, are stage 2. Parenchymal infiltrates with diminishing hilar adenopathy characterize stage 3. - Stage 4: Volume reduction, bronchiectasis, calcification, or cyst formation in parenchymal infiltrates . Peribronchial illness may be discovered by high-resolution chest CT scan. Cardiac PET scan may reveal cardiac sarcoidosis. Positron emission tomography (PET) scan can show areas of disease activity in the lungs, lymph nodes, and other places of the body. However, PET scan cannot distinguish between malignancy and sarcoidosis. Despite the fact that serum amyloid A and adenosine deaminase levels are raised in sarcoidosis, these tests are not employed in clinical settings because of their poor sensitivity and specificity. Other/Diagnostic Procedures PFTs for pulmonary function may show a restrictive pattern with lower DLCO for carbon monoxide diffusing capacity. Bronchoalveolar lavage fluid has a higher CD4-to-CD8 ratio when a disease is active. ongoing investigation on whether D-dimer levels in BAL contribute to the diagnosis of sarcoidosis. The results of an ophthalmologic examination may show conjunctivitis, uveitis, or retinal vasculitis. Tuberculin skin test, ECG, In the event that the lungs are afflicted, bronchoscopy with biopsy of the central and peripheral airways is beneficial. Biopsy of the lesions should demonstrate noncaseating granulomas. The diagnostic yield of transbronchial needle aspiration guided by endobronchial US (EBUS) may be higher. Kveim test (ongoing research): To elicit a sarcoid granulomatous response over three weeks, similar to a tuberculin skin test, sterilized splenic cells from a patient with sarcoidosis are injected into an intradermal skin test. Alert It is not required to do a biopsy if symptoms suggest Löfgren syndrome (acute sarcoid with bilateral hilar lymphadenopathy, EN, and generalized arthritis/arthralgias), as the prognosis is good with observation alone, and a biopsy would not modify care. Noncaseating epithelioid granulomas without signs of mycobacterial or fungi infection, according to the test interpretation Management No treatment may be necessary in those who are asymptomatic, but it may be necessary if the patient has cardiac, CNS, renal, or ophthalmic involvement. Many people experience spontaneous remission. No therapy is recommended but frequent follow-up is advised for asymptomatic patients with stage I to stage III radiographic abnormalities and normal or somewhat impaired lung function. The premise for treating pulmonary symptoms is impairment. - Decreasing lung function and pulmonary symptoms, as well as deteriorating radiographic findings Medication Hypercalcemia and diseases of the heart, brain, or eyes are suggested for systemic therapy. As many pulmonary sarcoidosis patients are asymptomatic or experience a spontaneous remission, the majority of patients do not need pharmacological treatment. Initial Line Systemic corticosteroids in symptomatic individuals or with deteriorating lung function or radiographic abnormalities; no FDA-approved treatment for sarcoidosis. - There is no established ideal glucocorticoid dosage. Tuberculosis must be ruled out before starting glucocorticoids. - Typically prednisone, 0.3 to 0.6 mg/kg ideal body weight (20 to 40 mg/day) for 4 to 6 weeks - if stable, taper by 5 mg/week to 10 to 20 mg/day during the following 6 weeks. - 10 to 20 mg per day for 8 to 12 months if there is no relapse. Relapse is typical. - Patients with acute respiratory failure, cardiac, neurologic, or ophthalmic illness may require higher doses (80 to 100 mg/day). Topical steroids may be useful in people with skin conditions. In cases with early illness and moderate pulmonary symptoms, inhaled steroids (budesonide 800 to 1,600 mg BID) may be of some therapeutic benefit. - Restrictions and important potential interactions: Consult the medication profiles provided by the manufacturers. Next Line All glucocorticoid substitutes have a significant risk of severe side effects, including myelosuppression, hepatotoxicity, and opportunistic infection. Examine for steroid compliance, concomitant disease, or other complicating reasons causing steroid failure before using these drugs. It is advised to refer patients to specialists. Methotrexate: start with 7.5 mg/week and work your way up to 10 to 15 mg/week. not to be used in cases of liver disease Azathioprine is typically taken in addition to prednisone in an effort to reduce steroid dosages. Use of immunosuppressants like methotrexate or azathioprine will necessitate routine CBC and LFT monitoring. Antimalarial drugs like chloroquine and hydroxychloroquine have undergone clinical trials without clearly showing any benefits. In circumstances where other treatments have failed, tumor necrosis factor antagonists like infliximab have been helpful. Referral If additional organ systems are involved, a pulmonologist may follow, with referrals to other specialists as necessary; if second-line therapy is required, a specialist should follow. Surgical Techniques In severe, refractory cases, lung transplantation may be necessary; long-term effects remain unknown. Take Action There is a lack of information regarding the best frequency for monitoring disease activity and the indications for particular testing. Followed by suggestions. Patient observation Prednisone users should be checked every one to two months while taking their medication. For the first two years after diagnosis, patients who do not need therapy should be examined every three months. During this time, a history and physical examination, as well as laboratory tests specific to the locations of disease activity, PFTs, and ambulatory pulse oximetry, should be performed. If the disease is active, get an eye exam every six to twelve months if you're taking hydroxychloroquine. - CBC, creatinine, calcium, LFTs, ECG, 25-hydroxy and 1,25-dihydroxyvitamin D, CXR, and ophthalmologic examination every year Additional tests based on the symptoms of each patient, such as a brain MRI, HRCT, echocardiography, Holter monitoring, urinalysis (UA), thyroid-stimulating hormone (TSH), and bone density Some doctors utilize the serum ACE level to monitor the progression of the illness. When receiving treatment or when the condition is treated, ACE levels in people who had initially increased levels should return to normal. If the illness is dormant, a history and physical examination, PFTs, ambulatory pulse oximetry, CBC, creatinine, calcium, liver enzymes, 1,25-dihydroxyvitamin D, ECG, and ophthalmologic exam should be performed annually. Prognosis: Within two years, 50% of patients will experience spontaneous resolution. After two years, 25% of patients will have considerable fibrosis but no further progression of the illness. 25% of patients will have a chronic illness (the percentage is higher in specific demographics, particularly Black Americans). Patients who have used corticosteroids for longer than six months are more likely to develop chronic conditions. 5% is the overall death rate. Patient complications such cor pulmonale and severe respiratory involvement are possible. Aspergillosis infection in the injured lung may cause pulmonary bleeding. Other organs, particularly the heart (congestive heart failure, arrhythmias), eyes (rarely blindness), and CNS, might be affected and suffer severe repercussions. Kembara Xtra - Medicine - Salmonella Infection Any serotype of the gram-negative, facultatively anaerobic Salmonella bacteria can cause infection. Nontyphoidal Salmonella commonly causes gastroenteritis through foodborne infection and sporadic outbreaks; it less frequently causes infection outside the gastrointestinal (GI) tract. - Nontyphoidal invasive illness - Enteric fever - Chronic carrier state (>1 year) - Nontyphoidal gastroenteritis • Bacteremia- Endovascular problems Localized infection outside the gastrointestinal tract (such as osteomyelitis and abscesses) Aspects of Geriatrics Due to comorbidities (atherosclerotic endovascular lesions, prosthesis, etc.) that enhance the likelihood of bacterial seeding, patients over 65 have an increased risk of invasive illness with bacteremia and endovascular sequelae. Child Safety Considerations Infants under three months old are more vulnerable to invasive illness and consequences. Epidemiology Incidence Global incidence of invasive nontyphoidal Salmonella infection estimated to be 535,000 cases in 2017. Most frequently identified foodborne bacterial illness in the United States and a common cause of traveler's diarrhea.Global incidence of nontyphoidal Salmonella enteritidis estimated to be 94 million per year (mostly foodborne).Wide variation by region from 40 to 3,980 estimated cases per 100,000 Highest incidence of bacteremia in children under the age of five; hospitalization rates are higher in patients over the age of fifty; estimated 1.4 million cases annually in the United States; annual incidence of 15 illnesses per 100,000; peak frequency: July to November; second-most common bacteria isolated from stool cultures in diarrheal illness in the United States (behind Campylobacter); highest incidence of bacteremia in children under the age of five; Pathophysiology and Etiology 2,500 distinct serotypes of Salmonella enterica, the most virulent species in humans. 95% of cases are foodborne in terms of etiology. - Additional cases (5%) are caused by direct or indirect oral contact with animal or human carriers who have the disease. - Iatrogenic contamination, such as that caused by blood transfusion or endoscopy, is uncommon. Pathophysiology - In immunocompetent patients, a typical infectious dosage is 1 million bacteria; however, this dose can be reduced in patients who are taking antibiotics or when there is a reduction in gastric acid. - When bacteria are consumed, they infiltrate the proximal and distal colonic mucosa, triggering an inflammatory and cytotoxic reaction. - Bacteria can cause invasive or disseminated illness by entering the mesenteric lymphatic system and later the systemic circulation. Risk factors include recent travel to developing countries and the consumption of raw meat, raw eggs, and raw dairy products. Products made from non-animals have also been linked to epidemics. Impaired gastric acidity is caused by H2 receptor blockers, antacids, proton pump inhibitors (PPIs), gastrectomy, achlorhydria, pernicious anemia, newborns, and contact with live reptiles or fowl. Immunosuppression due to HIV, diabetes, corticosteroid or other immunosuppressant use, chemotherapy, recent antibiotic use, reticuloendothelial blockage from sickle cell disease, malaria, or bartonellosis, impaired phagocytic function from hemoglobinopathies, malaria, and chronic granulomatous illness. Age of 5 years or older. Basic Prevention Proper sanitation throughout food production, transportation, and storage (such as using refrigeration and fully boiling food before consumption); Control of animal reservoirs: Maintain good hand hygiene; the CDC monitoring outbreaks (http://www.cdc.gov/salmonella/); and stay away from high-risk animals, feces, and polluted rivers. Accompanying Conditions Gastroenteritis, Bacteremia in immunocompromised individuals or individuals with underlying conditions (such as cholelithiasis, prosthesis), Osteomyelitis in people with sickle cell disease, Abscesses in people with malignant tumors, and Rheumatoid arthritis. Salmonella infections are frequently asymptomatic or cause mild, self-limiting gastroenteritis. Exposure history includes travel, contact with sick people or animals, and faulty food preparation. Age, immunological health, and other risk factors are considered hosts. In most cases, symptoms appear 8 to 72 hours after intake and go away in 4 to 10 days. Acute, simple disease with sudden onset of diarrhea that is not usually horrifyingly bloody but can be, especially in young individuals. - Vomiting is not common. - Cramps in the abdomen - Headache - Myalgias - Fever Clinical Examination: Fever; Hypovolemic Signs; Tenderness in the Abdomen; Some Patients Have Heme-Positive Stool; Some Patients Have Hepatosplenomegaly Differential diagnoses include pseudomembranous colitis, bacterial enteritis caused by other organisms, viral gastroenteritis, and inflammatory bowel disease. Laboratory Results Initial examinations (lab, imaging) Stool culture for Salmonella, Escherichia coli, Shigella, and Campylobacter in cases of gastroenteritis (the ideal specimen is a sample of diarrheal stools.) - Stool cultures may be indicated for the following reasons: Serious diarrhoea (6 or more loose stools per day).Fever, bloody or mucous-filled diarrhea, many instances pointing to an outbreak, diarrhea lasting more than a week, and a positive fecal leukocyte test - Blood cultures are recommended for anyone who exhibits indications of septicemia or other systemic manifestations of an infection, is under three months old, has a suspected case of enteric fever, or is immunocompromised. Bacteremia may manifest as fever blood cultures and/or positive stool cultures. If the patient is under three months old and has a positive blood culture, culture the CSF. Endovascular infection: If an aortic or vascular cause is suspected in bacteremic patients older than 50 years old, consider angiography. Consider CT or MRI for infections of soft tissue or bones. Local infections-Wound culture. Chronic carriers may have positive urine cultures if their stool cultures have been positive for more than a year. Further Tests When diarrhea lasts longer than 14 days, look for additional causes. Salmonella excretion may continue asymptomatically for weeks after infection; hence, follow-up fecal cultures are ordinarily not advised for patients with simple gastroenteritis. Blood cultures should be taken again if a patient has bacteremia. Interpretation of Tests If intestinal biopsies are performed, they may reveal reticuloendothelial hypertrophy/hyperplasia as well as mucosal ulceration, bleeding, and necrosis. Management For immunocompetent individuals between the ages of 12 months and 50, the recommended course of treatment for nonsevere nontyphoidal Salmonella gastroenteritis is supportive care. Usually, the sickness has a limited lifespan. The value of treating minor illnesses has not been established. The immune response of the host can be suppressed by treatment. Additionally, higher relapse rates have been noted, and asymptomatic carriage may last longer. In immunocompetent hosts who have severe diarrhea, a high fever, or who need hospitalization, take antibiotics into consideration. ● Antibiotics are beneficial for patients with bacteremia: Patients >50 years old (Risk significantly rises after age 65) - Infants under 3 months - Patients under 3 months. Patients with hemoglobinopathies, atherosclerotic lesions, prosthetic valves, grafts, or joints, as well as those who are immunosuppressed or have HIVSalmonella not typhoidal chronic carriage - 4 to 6 weeks of antibiotic therapy - Prophylactic treatment in immunocompromised people Hand washing and barrier precautions for inpatients.Hydration and electrolyte replacement. When a patient has a fever or dysentery, antimotility medications should be avoided. Antimotility medications may prolong the time the enteropathogen is in touch with the gut mucosa. First Line of Medicine Uncomplicated gastroenteritis: Supportive care is all that is required; no special drugs are required. Complicated gastroenteritis (owing to sickness severity or host risk factors like immunosuppression) – Adults (If immunocompromised, treat for 14 days.) Levofloxacin: 500 mg once daily orally for one to three days. Ciprofloxacin: 750 mg daily, orally, for one day; 500 mg daily, orally, for three days. 400 mg/day, orally, for 1 to 3 days, of ofloxacin Azithromycin: 500 mg/day PO for 3 days, or 1 g, then 500 mg per day for 3 days. Children's preferred treatment for febrile diarrhea or dysentery .Ceftriaxone: two equally spaced doses of 100 mg/kg/day IV or IM for seven to ten days, or Azithromycin: 10 mg/kg/day for the following dosages over the course of seven days after the initial dose of 20 mg/kg PO. AIDS patients Increased antimicrobial therapy duration (between 2 and 6 weeks) and/or zidovudine use may reduce relapse. Bacteremia: Due to trends in resistance, life-threatening infections in adults should be treated with fluoroquinolones or third-generation cephalosporins until susceptibilities are established. – Adults 400 mg IV BID for 10 to 14 days of Ciprofloxacin (or another fluoroquinolone) + Ceftriaxone: 1–2 g intravenously every day for 10–14 days, or Children: Cefotaxime: 2 g IV every eight hours for 10 to 14 days Trimethoprim-sulfamethoxazole: 8 to 12 mg/kg/day of the trimethoprim component in 2 divided doses for 10 to 14 days or Amoxicillin: 30 mg/kg/dose TID for 10 to 14 days 50 mg/kg/day (maximum 1 g) BID for 10 to 14 days of ceftriaxone Localized infection (such as pneumonia, cholangitis, osteomyelitis, and septic arthritis); surgical drainage or débridement in addition to at least three weeks of antibiotic treatment - For 4 to 6 weeks, administer antibiotics orally to patients with immunocompromised patients, chronic local infections, or sustained bacteremia. Chronic carrier status (shedding for more than a year) Ciprofloxacin: 500 mg PO BID for 4 weeks; Levofloxacin: 500 mg/day for 4 weeks; Norfloxacin: 400 mg PO BID for 4 weeks if gallstones are present. Amoxicillin: 1 g PO TID for 12 weeks. Trimethoprim-sulfamethoxazole: 160 mg/800 mg PO BID for 12 weeks. Caution Resistance to antibiotics .There have been reports of strains that are resistant to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole. Fluoroquinolone resistance is rising, possibly as a result of the drugs' expanding use in animals. There have been more and more reports of extended-spectrum cephalosporin resistance. Next Line Aztreonam is an alternate medication that may be helpful for people who have several allergies or if the organism exhibits an unusual pattern of resistance. Fluoroquinolones are currently frequently administered to kids for 5 to 7 days in regions of the world where Salmonella typhi is frequently multidrug resistant. Surgical Procedures If biliary tract disease is present, a preoperative 10- to 14-day course of parenteral antibiotics is advised prior to cholecystectomy. Surgical excision and drainage for contaminated tissue areas, followed by a minimum of 3 weeks of antibiotic therapy. Patient Follow-Up Monitoring Salmonella can shed asymptomatically for weeks after infection. Patients with simple gastroenteritis typically don't need follow-up fecal cultures. During a Salmonella outbreak, requirements might change. State and local laws may have different requirements. Some public health agencies demand negative stool cultures before allowing medical personnel and food handlers to resume their jobs. It can take 4 to 8 weeks to finish shedding. Public health laboratories can perform serotyping on isolates. Diet Simple to digest food Modification of Lifestyle Careful hand washing and handling of raw meat, poultry, and eggs Before eating, fruits and vegetables should be well cleaned. Salmonella is eliminated from meats by thorough cooking. Use caution while handling animals that have high incidences of fecal carriage. Salmonella gastroenteritis typically has a good prognosis and a self-limited course. The elderly (>65 years), the immunocompromised, and the young (3 months) all have higher mortality rates. Mortality is increased in multidrug-resistant strains, and is associated with bacteremia and other invasive infections. Complications Endocarditis, infectious endarteritis, meningitis, septic arthritis, reactive arthritis, osteomyelitis, pneumonia, appendicitis, cholecystitis, toxic megacolon, hypovolemic shock, metastatic abscess development Kembara Xtra - Medicine - Salivary Gland Calculi / Sialadenitis One or more salivary glands are inflamed. It can be autoimmune, obstructive, or infectious. When eating, the affected gland experiences a painful swelling known as "sialolithiasis" that is brought on by a blockage of the salivary glands or ducts by a stone. "Sialadenitis" is an inflammation of the salivary gland that can be either acute or chronic. A primary infection (viral/bacterial) or secondary infection may be the source of acute. Repeated episodes of inflammation that lead to a progressive decrease of salivary gland function are what cause chronic sialadenitis. Sialadenitis frequently affects the submandibular glands and the parotid gland. However, acute suppurative sialadenitis is the main cause of parotid gland inflammation. Due to the higher mucinous content of saliva, longer Wharton duct course, and slower salivary flow against gravity, the submandibular gland is more frequently (80–90% of cases) impacted by stones than the parotid gland. Peak incidence is between the ages of 30 and 60; children are rarely affected. Patients who are weak and dehydrated are more likely to develop salivary stones, which are 70% solitary and 30% bilateral. Pathophysiology and Etiology Elevated calcium concentrations and stagnation of salivary flow are suggested to be significant. Reduced salivary output brought on by anticholinergic medications, dehydration, or radiation . Predisposing factors for salivary calculi include inflammation of the salivary gland or duct, salivary stasis, retrograde bacterial contamination from the oral cavity, increased salivary alkalinity, and physical trauma to the salivary duct or gland. Salivary calculi are composed of calcium phosphate and hydroxyapatite with smaller amounts of magnesium, potassium, and ammonium. The development of salivary stones and gout. Sialoliths in gout are made of uric acid. Staphylococcus aureus, Streptococcus viridans, Streptococcus pyogenes, Haemophilus influenzae, Escherichia coli, Pseudomonas aeruginosa, and group B streptococci (neonates and children) are the most common bacteria to cause sialadenitis. Because of the mumps, CMV, Epstein-Barr virus, HIV, and enteroviruses, viral sialadenitis frequently has several foci. The use of radioiodine, positive pressure ventilation when under anesthesia, Sjögren syndrome, and sarcoidosis are some additional common reasons. Child Safety Considerations Idiopathic juvenile recurrent parotitis and the mumps are frequent causes of sialadenitis in kids. Anticholinergic usage, poor oral hygiene, hunger, smoking, dehydration, and head-and-neck radiation are risk factors. Prevention Avoid anticholinergics and other xerostomia triggers, and practice good oral hygiene. Associated Conditions Sjögren syndrome, Mikulicz syndrome, radiation or medication-induced xerostomia, and hypercalcemia Diagnosis The submandibular glands account for the majority (80%) of salivary gland stones, followed by the parotid gland (6–20%) and the sublingual or small salivary glands (1–2%). The duct is where submandibular stones are more frequently found. Stones in the parotid gland are internal to the gland itself, more numerous, and often smaller than stones in the mandible. History Acute onset of pain and swelling over the affected salivary gland, especially postprandial or following the anticipation of eating; dental pain, discharge, bad breath (halitosis); hypersalivation; and pain with chewing; review history for: alcoholism, bulimia, malnutrition; radiation therapy, past malignancy; TB or HIV exposure; Xerostomia Worsening discomfort, erythema, and/or fever may indicate secondary infection Pus drainage from the gland duct into the mouth 33% of patients with submandibular sialolithiasis present with painless swelling and 10% with pain but not swelling. Clinical evaluation Visual examination of the glands and ducts may reveal a stone in the Wharton duct or close to the tongue's frenulum in the case of the submandibular gland. A stone for the parotid glands may be felt in the Stensen duct or observed at the aperture. Bimanual examination of the oral cavity, including palpation of all salivary glands, the tongue, the floor of the mouth, and the neck to determine symmetry, tenderness, induration, edema, the presence of stones, lymphadenopathy, and the number of affected glands. Typically, an active gland is elastic and spongy. Check the duct apertures for saliva and purulent discharge. It is possible to have acute bacterial sialadenitis if there is a purulent discharge from the opening. Gently palpate the gland to check for normal, thin, nonexistent, or diminished saliva production and to feel for bubbling or purulent outflow. Look into interstitial keratitis in the eyes. An assessment of the facial nerve's (CN VII) health, which could be jeopardized if the parotid gland is affected. Child Safety Considerations Children's stones frequently occur within the distal duct. In sialendoscopy, ultrasound is both diagnostic and therapeutic. Differential diagnosis include salivary gland cancers, lymphoma, cystic fibrosis, bacterial parotitis, idiopathic juvenile recurrent parotitis, the measles, and tularemia. Laboratory Results Sialolithiasis is diagnosed clinically based on a distinctive history and physical exam. When eating or anticipating eating, the afflicted gland often experiences an abrupt onset of pain and swelling. At the damaged salivary duct's opening or throughout its length, a stone could be palpable. Initial examinations (lab, imaging) Think about CBC. Culture and sensitivity of any expressed pus. Up to 90% of stones 2 mm or larger can be found with ultrasound. The CT scan with IV contrast is more sensitive, but it exposes you to radiation. MR sialography without intraductal contrast for patients with an inconclusive ultrasound and persistent symptoms. Sonopalpation, which combines transoral palpation with ultrasound, has a sensitivity and specificity of 96.6% and 90% for detecting calculi, respectively. Tests in the Future & Special Considerations Request rheumatoid factor (RF) and antinuclear antibodies (ANAs) tests if an autoimmune disease is suspected. Diagnostic Procedures/Other: Salivary gland biopsy .Sialography to assess obstructive lesions such as sialolithiasis. Sialoliths can be found and removed through sialendoscopy. In one investigation, sialendoscopy verified 812 (93%) submandibular stones and 221 (79%) parotid stones. According to one study, sialendoscopy, cone beam CT, and sonography all exhibited great specificity and positive predictive value when it came to identifying stones. A unique ultrasound-guided needle localization method has been suggested when sialendoscopy fails. Patients with sialolithiasis had decreased gland excretion and decreased absorption, according to technetium-99m pertechnetate scintigraphy. Management Keep yourself hydrated. Use hot compresses. Milk the duct while massaging the gland. Sialagogues, or substances that encourage salivation, may be beneficial. Examples include tart, lemon juice, and hard candies (lemon drops). Use as tolerated throughout the day. Practice proper oral hygiene. By using mouthwash containing chlorhexidine 0.12% three times a day, you can improve oral hygiene and lessen the amount of germs that live in your mouth. Stop using drugs that have anticholinergic effects and lower saliva production. Prescription drugs include NSAIDs for pain relief and antibiotics for any secondary infections (fever, purulent discharge). Initial Line A culture of the duct discharge should be collected, and the antibiotic coverage should be expanded by switching to amoxicillin/clavulanate or clindamycin if there is no improvement after 5 to 7 days. Antistaphylococcal antibiotics such dicloxacillin or cephalexin 500 mg QID for 7 to 10 days. Clindamycin 300 mg PO every 8 hours if you are allergic to penicillin. Fluoroquinolones or third-generation cephalosporins for Gram-negative bacteria Metronidazole or clindamycin for anaerobic bacteria Next Line For empiric coverage, first-generation cephalosporins (cephalexin or cefazolin) or clindamycin are also recommended. Vancomycin in the event of MRSA If you have a dental abscess or poor dentition, consult a dentist. ENT if symptoms recur or don't go better with conventional treatment Further Treatment Consider placing a sialostent in the case of chronic sialadenitis with strictures. Surgical Techniques Submandibular stones in the hilum require gland excision, but those on the anterior floor of the mouth can be removed intraorally (sialodochoplasty). Parotidectomy is typically necessary for parotid stones. Sialadenitis and sialolithiasis treated by sialendoscopy have shown promising results in terms of symptom reduction, patient quality of life, and safety. Strictures, ranulas, and lingual nerve damage are complications. Sialendoscopy is not advised in cases of severe sialadenitis. A combination strategy employing sialendoscopy and a small intraoral incision had an 86% success rate. When conventional treatment for a parotid abscess fails after three to five days, surgery is required to drain the abscess. ● In about 80% of instances, sialoliths larger than 4 mm and stenoses can be successfully treated using radiologically, fluoroscopically, or sialendoscopically based techniques. Up to 50% of patients who undergo extracorporeal shock wave lithotripsy (ESWL) are successful. 90% success rate with transoral duct cutting for extraparenchymal submandibular stones Alternative Therapies To encourage salivation, consider using lemon drops or other sialogogues. In one study, sialogogue use after surgery nearly cut sialadenitis incidence in half. Admission Parotid abscess and inability to tolerate PO intake Avoid recommending drugs that contribute to xerostomia. Keep an eye on patients with chronic sialadenitis since acute exacerbations might result from diminished salivary gland function brought on by fibrosis and acini loss. Diet Avoid sialogogues during acute bouts, and drink enough water. Modification of Lifestyle preserving healthy dental and hydration habits With the right care, acute symptoms will often go away in about a week. Following cautious outpatient care, full recovery is anticipated. Due to systemic involvement, patients with autoimmune etiology may experience a longer course. 18% of individuals who have transoral surgery to remove stones have reported experiencing a recurrence. Complications Localized infection that spreads, leading to cellulitis or Ludwig's angina; facial nerve impingement; hypoglossal and lingual nerve injuries; and dental decay because salivary gland hypofunction reduces teeth's ability to fend off acid erosion and decay. Kembara Xtra - Medicine -Rotator Cuff Impingement Syndrome The most frequent cause of non-traumatic shoulder discomfort in those over 25 is compression of the rotator cuff tendons and subacromial bursa between the humeral head and the components of the coracoacromial arch and proximal humerus. The "painful arc"—a range of arm abduction between 60 and 120 degrees—is when pain is felt the maximum. Traditionally broken down into three stages: - Stage I: Acute inflammation, edema, or bleeding of the underlying tendons as a result of overuse (mostly affects those under 25 years old) - Stage II (often affecting people between the ages of 25 and 40): progressive tendinosis that causes a partial rotator cuff tear and underlying thickening or fibrosis of the surrounding structures. - Stage III: complete thickness tear (common in patients older than 40 years) Incidence 1% of all visits to the doctor for primary care are for shoulder pain. Patients between the ages of 42 and 46 had a peak incidence of 25/1,000 patients each year. Impingement is the diagnosis for 18–74% of shoulder pain cases. Prevalence In the general population, shoulder pain can occur anywhere between 7% and 30% of the time. Risk factors include shoulder trauma, thickened coracoacromial ligament, repetitive overhead motions (throwing, swimming), glenohumeral joint instability, muscle imbalance, acromioclavicular arthritis, and smoking. Prevention Proper lifting and throwing mechanics, and balanced rotator cuff and scapula stabilizer muscle development are all important. Increasing shoulder pain gradually with overhead activity is the diagnosis (A tear is suggested by a sudden start of intense pain.) Night pain is frequent and made worse by sleeping with the affected arm over the head or laying on the affected shoulder. Anterior shoulder soreness when performing overhead motions If the shoulder is not used through its entire range of motion, it could lead to weakness and limited range of motion. Clinical evaluation Check the patient for asymmetry or atrophy. Watch the patient remove his or her shirt during the examination. Neer impingement test: The scapula is stabilized while the afflicted upper extremity is moved in an arc of flexion by the examiner. Positive is shoulder flexion-related pain. 78% sensitivity. Particularity: 58% The Hawkins-Kennedy impingement test involves the examiner flexing the arm 90 degrees forward before gradually rotating the arm internally. When the patient experiences discomfort or the examiner feels or observes the scapula rotating, that is the internal rotation's end point. When the patient feels discomfort while performing the test, it is considered positive. 74% sensitivity. Particularity: 57% Empty can test (supraspinatus): The patient is instructed to elevate and internally rotate their arm while pointing their thumbs in the direction of their scapula. Elbow should be extended all the way. The examiner presses downward on the arm's top surface. When the patient expresses pain while showing resistance, the test is affirmative. 69% sensitivity. 62% specificity The lift-off test (subscapularis) requires the patient to internally rotate their shoulder while placing the back of their hand on the buttock on the opposite side, and then to raise that hand off against resistance. This motion becomes weak when the subscapularis muscle is torn. 42% sensitivity. 97% specificity Patient fully rises arm and then gently reverses motion in the drop-arm test. The test is positive for a potential rotator cuff tear if the patient experiences severe discomfort or drops their arm abruptly. 21% sensitivity. 92% specificity Resisted external rotation: teres minor and/or infraspinatus tendon involvement-related weakness . Test for anterior glenohumeral joint instability using apprehension-relocation: Have the patient lie on his or her back or sit as the examiner slowly rotates the humerus (pushing the hand posteriorly while the patient resists and then anteriorly while the patient resists). The test is positive if the patient has any anxiety or worry as a result of this movement, indicating instability and a potential for dislocation. Instead of focusing on instability if pain is present, think about labral tears and/or impingement syndrome. To rule out cervical pathology as the cause of shoulder pain, examine the cervical spine. Upper-limb neurovascular examination Multiple Diagnoses Labral injury The pain when the affected arm is fully adducted across the chest in a horizontal plane is a sign of acromioclavicular arthritis, which is more common in elderly people. Adhesive capsulitis (rotator cuff tendonitis causes the muscles in the rotator cuff to become less active, atrophy, and eventually constrict; associated with diabetes and maybe previous trauma) Anterior shoulder instability (previous trauma; individuals under 25 are more likely to have it) Instability in multiple directions .Perform the Speed and Yergason tests and search for a visible or palpable deficiency in the biceps, often known as the "Popeye sign." Calcific tendinitis and cervical radiculopathy (which can be tested with the Spurling maneuver if there is spinal or foraminal stenosis) Glenohumeral arthritis (Question using simple films.) Suprascapular nerve entrapment (observe focal infra- or supraspinatus muscle atrophy). Rotator cuff tear caused by trauma Initial test results from the laboratory and imaging Anteroposterior, axillary, and scapular Y views of the shoulder on plain-film radiographs. Plain films may show: - Acromioclavicular and glenohumeral joint osteoarthritis - Superior migration of the humeral head (a sign of a significant rotator cuff injury) - Cystic alteration of the humeral head and inferior acromion sclerosis (signs of chronic rotator cuff illness) - Tendinitis calcific MRI is utilized to conclusively assess partial tears, full tears, and tendinopathy of the rotator cuff. Ultrasound is sensitive and selective for rotator cuff injuries but is extremely operator dependant. MR arthrogram is preferable for labral disease. For patients who cannot receive an MRI or who have bone disease, a CT scan is suggested. Lidocaine injection test: Inject lidocaine into the subacromial region as part of diagnostic procedures or other: Repeat the impingement tests; if the pain is fully gone and your range of motion increases, it's probably impingement syndrome and not a rotator cuff injury. - Makes physical examination strength testing more accurate: If strength is intact, a rotator cuff tear can be ruled out. If range of motion does not improve in any plane, adhesive capsulitis is more likely to be the cause. After a lidocaine injection with some improvement in range of motion .A lack of pain alleviation may indicate additional origins (such as cervical radiculopathy) or ineffective injection placement. Glenoid labral tear; capsular strain; glenohumeral osteoarthritis; glenohumeral instability. Interpretation of Tests may have a muscle or tendon injury, tendonitis, or tendinosis. Management Most patients' rotator cuff tendonitis improves and completely cures with pain management and vigorous therapy. Ice or heat for discomfort alleviation; rest initially; afterwards, physically supervised rehabilitation is required for 6 to 8 weeks; activity modification with avoidance of aggravating activities, particularly overhead motions; Strengthening the muscles around the rotator cuff will improve stability and help to prevent further injuries. Range of motion exercises. First-line treatment with NSAIDs or another analgesic, often for 6 to 12 weeks Referral failure of conservative therapy, ongoing discomfort, weakened condition, or rotator cuff injury in its entirety Exercise programs under supervision or performed at home significantly reduce pain and enhance function. Physical therapy is successful for both short- and long-term function rehabilitation. After the pain has subsided, gradually strengthen the rotator cuff muscles that control internal rotation, external rotation, and abduction. Surgical Procedures Although they do not appear to have a substantial long-term impact, steroid injections may significantly improve pain and function in the short term. There is no proof that surgery is better for impingement syndrome than conservative therapy or that one surgical technique is superior to another. Platelet-rich therapy for soft tissue musculoskeletal injuries are becoming more and more popular. - The use of platelet-rich plasma during arthroscopic rotator cuff surgery does not appear to have any impact on overall retear rates or shoulder-specific results. Extracorporeal shock wave therapy is a newly discovered method of treating calcific tendinitis, and it is actively being researched. Healthcare Alternatives Acupuncture may help with pain management and function enhancement, especially when combined with physical therapy. Constant Care Physical therapy, home exercises, and surgical intervention all require physical rehabilitation. This is true for both conservative and surgical treatment modalities. Prior to comprehensive testing or surgical intervention, an intensive trial of rehabilitation should be recommended. Getting rid of discomfort before starting a physical therapy program enhances compliance and results because symptoms frequently return if not entirely treated. Variable prognosis that relies on the underlying pathology .The majority of patients get better with conservative treatment. Recovery may take time. Patients who have had more severe symptoms for longer than a year are less likely to benefit from conservative therapy. Tendon retraction in a full rotator cuff tear is one of the complications. Injury progression is another. Kembara Xtra - Medicine - Roseola Infection that is pervasive in childhood and early life. Human herpesvirus 6 (HHV-6) is responsible for the majority of instances and may be linked to other illnesses, such as encephalitis. Acute infection in newborns or young children causes a high fever, which is followed by a skin eruption when the fever subsides. Transmission occurs when saliva or respiratory droplets come into touch with the patient. Skin/exocrine, metabolic, gastrointestinal, respiratory, and neurologic system(s) involved. Incubation period of 9 to 10 days. Synonym(s): pseudorubella; sixth disease; 3-day fever Epidemiology: Peak age of infection is 6 to 9 months, with congenital or prenatal infection being rare. Predominant age group for HHV-6 is infants and young children (under 2 years old).By the age of two, 95% of children had contracted HHV-6. - HHV-7 - Later childhood - Mean age of infection 26 months - More than 90% of the population has HHV-7 by 10 years - Predominant sex: male = female - No seasonal variation Common—represents 20% of ED visits for febrile illness in children aged 6 to 8 months. Prevalence Between 9 and 21 months is when prevalence peaks. By three years, almost all people had HHV-6. Roseola affects 20% of people with primary HHV-6. Pathophysiology and Etiology HHV-6 and HHV-7 HHV-6B is more common than HHV-6A in the majority of cases (60–74%) - HHV-6A detected in young African youngsters - All nucleated cells have CD46 receptors, which HHV-6 attaches to. Primary infection usually caused by saliva or respiratory droplets .1% of instances involve congenital infection or vertical transfer. - Transmission transplacentally - Chromosomal integration (unknown clinical relevance) . After primary infection, a lifelong latent or persistent asymptomatic infection develops. - 80–90% of the population sporadically excretes HHV-6 and HHV-7 in saliva. - Patients are viremic from two days prior to the commencement of a fever to the onset of defervescence and rash. - The CSF is also connected to HHV-6 latency. Genetics 0.2–3.0% of the population has HHV-6 incorporated into their chromosomes. The virus spreads vertically as a result of this. This's clinical relevance is unknown. Risk factors include being a woman, having elder siblings, being immunocompromised, and having had a bone marrow transplant (BMT), among other solid organ transplants. In the first week following a transplant, HHV-6 reactivation is possible. 30-45% of BMT develop HHV-6 viremia within the first several weeks of transplantation. Most often asymptomatic HHV-6 reactivation/reinfection rates as high as 82% in solid organ transplant The child may be fussy throughout this prodrome. Diagnosis: 3 to 5 days sudden fever 102.2-104.0°F (39-40°C) not linked with a rash. A rash that first appears on the trunk then spreads centrifugally to the neck, probably the face, and possibly the extremities is connected with a sudden drop in temperature. Mild upper respiratory symptoms, including diarrhea.In 13% of cases of rhinorrhea, febrile seizures happen. Clinical evaluation Exanthem subitum, Rash - Rose-pink papules and/or macules that blanch - show on the trunk first, then spread outward - May show up to 3 days after the fever goes away - Fades in 2 days - Affects 20% of patients in the USUlcers on the soft palate and uvula (Nagayama spots) Mild tympanic membrane, throat, and/or conjunctival irritation Cervical lymphadenopathy Periorbital edema Differential diagnosis: Rubella, scarlet fever, drug eruption, measles, enterovirus infection, adenovirus infection, Epstein-Barr virus, and parvovirus B19. Laboratory Results Tests frequently cannot distinguish between a latent or active disease, making the diagnosis primarily clinical and not requiring laboratory or radiologic evaluation. Only in extreme cases, an exact diagnosis is required; in cases of uncertainty, a more dangerous condition must be ruled out before considering antiviral therapy. Initial examinations (lab, imaging): PCR detection of HHV-6 and HHV-7 in serum, whole blood, CSF, or saliva if indicated. - Increasing in popularity - Not necessary in people who are not immunocompromised IgM immunofluorescence for HHV-6HHV-6 IgG immunofluorescence - Check at diagnosis and then again two weeks later. Diagnostic for acute infection - Spike noticed in the first week of sickness. - To demonstrate primary infection, use with IgM. - Primary infection is suggested by a negative initial test and an increase on follow-up. Other laboratory results include decreased total leukocytes, lymphocytes, and neutrophils, elevated transaminases, and thrombocytopenia. Viral culture is rarely performed, has no clinical utility, and takes a lot of time. Other/Diagnostic Procedures Chest x-ray (CXR): if a kid exhibits respiratory symptoms; urine culture: to rule out UTI as the cause of fever Management Treatment is not required, and there are no aftereffects General Actions Hydration and symptom alleviation, especially antipyretics First Line of Medicine No specific first-line therapy, other than supportive measures, is available in immunocompetent hosts. Antivirals are not advised for immunocompetent patients. There is no approved antiviral therapy for immunocompromised people. HHV-6B susceptible: ganciclovir and foscarnet; HHV-6A and HHV-7 are more resistant to ganciclovir. Second-line IV ganciclovir, cidofovir, and foscarnet tested in vitro investigations in stem cell transplant patients. Antivirals have been recommended in specific cases of encephalitis (linked to reactivation of HHV-6) Ganciclovir prophylaxis is effective in avoiding HHV-6 reactivation in bone marrow and stem cell transplant recipients who are receiving immunosuppression. Patient Follow-Up Monitoring In the febrile prodrome, keep an eye out for dehydration. None once the normal rash develops and the fever goes away. The average ailment lasts six days. If febrile seizures happen, they will stop after the fever goes down and are unlikely to happen again. Reactivation of symptoms in immunocompromised Encourage water in the diet. Parental assurance that this is typically a benign, self-limited condition through patient educationNo particular time frame for excluding affected children from outside-of-home care is advised. Prior to the beginning of fever and up until the period of defervescence and rash, the patient is viremic. Reactivation in immunocompromised people is prevalent. Course: acute, full recovery without sequelae. Complications 1/3 of all primary seizures in children under the age of two are caused by febrile seizures, which affect 13% of kids with roseola. Reactivation can happen in transplant patients, those with HIV infection, and other immunocompromised people. Medication hypersensitivity syndromes (drug reaction with eosinophilia and systemic symptoms). Meningoencephalitis affects immunocompetent and immunosuppressed patients, and there is little correlation between it and multiple sclerosis. Pityriasis rosea may be related to progressive multifocal leukoencephalopathy. Kembara Xtra - Medicine - Rocky Mountain Spotted Fever The most prevalent form of spotted fever rickettsiosis (SFR) in North America is called Rocky Mountain spotted fever (RMSF). Of all reportable rickettsial infections in the US, it is linked to the greatest incidence of severe and fatal consequences. The bacteria Rickettsia rickettsii is the cause of RMSF, a systemic small and medium vessel vasculitis spread by ticks. Starts in the wrists and ankles and spreads to the palms, soles, and trunk; symptoms include fever, headache, and myalgia as well as cardiovascular, musculoskeletal, cutaneous, central nervous system (CNS), renal, hepatic, and pulmonary system(s) impacted Epidemiology Ticks serve as both primary reservoirs and vectors in the United States. The Rocky Mountain wood tick, Dermacentor andersoni, is found in the western United States, the American dog tick, Dermacentor variabilis, is found in the eastern two-thirds of the country, and the brown dog tick, Rhipicephalus sanguineus, is found in every state. Incidence The annual incidence of SFR in the United States grew from 1.7 cases per million people in 2000 to 13.2 in 2016. All states, with the exception of Alaska and Hawaii, have reported cases. Over 50% of SFR instances occur in Arkansas, Missouri, North Carolina, Tennessee, and Virginia; RMSF is also detected in Canada, Mexico, and all of Central and South America. In Arizona, cases that hadn't previously been found there have also been found. Cases happen all year long. The peak months for outdoor activities are May through August, when most cases are documented. The highest incidence occurs in people between the ages of 60 and 64. Children under the age of 10 had the highest recorded death rate. Prevalence 4,470 instances were reported in the USA in 2012. Only 0.1% of ticks are carriers of dangerous rickettsial species. Pathophysiology and Etiology After 6 to 10 hours of eating, a mature tick discharges R. rickettsii from its salivary glands. Pathogens infect vascular endothelial cells, resulting in small and medium artery damage throughout the body and disseminated inflammation. Vascular permeability later on can result in cerebral and pulmonary edema. Platelet ingestion locally causes a distinctive petechial rash. Meningoencephalitis, ARF, acute respiratory distress syndrome, shock, arrhythmia, and seizures can also be brought on by subsequent end-organ injury. Symptoms start to show up 3 to 12 days after the bite or between 4 and 8 days after the tick was found attached. R. rickettsii may cross the placenta and infect the fetus, however this is uncertain. Rarely, direct tick blood injection into open wounds or conjunctivae might result in RMSF. Risk factors include exposure to the outdoors frequently or living in wooded regions; coming into contact with outdoor pets or wild animals; and having a tick that has been engorged or present for more than 20 hours. Basic Prevention Wear light-colored clothing, long sleeves, pants, socks, and closed-toe shoes to minimize tick exposure; tall grasses, open regions with low bushy vegetation, and woodland areas have the highest tick exposure. Use insect repellents with DEET. Spraying permethrin on garments .Regular tick checks, timely and correct tick removal, and never touch ticks with bare hands. Following tick removal, wash hands and the bite site with soap and water to prevent the possibility of mucosal inoculation. Diagnoses Regardless of a prior history of tick exposure, have a high index of suspicion for rickettsial infections in patients who present with "flu-like" symptoms in the summer. Delaying empirical therapy raises the risk of mortality and long-term consequences. History Consider RMSF if you experience an acute febrile fever and rash, especially if you have traveled to an endemic location or engaged in outdoor activities during the late spring or summer and have a history of possible tick exposure within the previous 14 days. 30% to 50% of the time, a tick bite goes unnoticed. Usually begins with sudden development of fever, severe frontal headache, malaise, myalgia, anorexia, nausea, vomiting, and photophobia within the first 1 to 4 days, mimicking a viral infection. Rash often develops 2 to 4 days after the start of a fever; it first shows as small, pink macules that blanch before spreading to the trunk, where it may take on a maculopapular appearance. Palm and sole involvement, which typically appears by the fifth or sixth day, is accompanied by a widespread petechial rash and is a symptom of severe disease. Rash typically spares the face. Even while children under 15 years old have rashes more commonly (>90%), only around 60% of children with RMSF have the traditional triad of fever, rash, and tick bite. 10% of patients never experience a rash, hence the appearance of a rash should not be the deciding factor in treatment. Conjunctival injection, mental status changes, restlessness, arthralgia, peripheral or periorbital edema, leg discomfort, and hearing loss are further symptoms. Clinical evaluation The normal rash begins as an erythematous, macular, or maculopapular exanthema (1 to 5 mm in diameter); 50% progress to petechial or purpuric lesions. The typical fever is >102°F. On dark skin, the rash may be difficult to see. In severe cases, the rash may cover the entire body, including the mucous membranes, and it may develop into necrotic or gangrenous lesions. The rash is not accompanied by urticaria or pruritus. AMS, lymphadenopathy, hepatosplenomegaly, generalized right upper quadrant discomfort, and edema on the palms or soles of the feet Differential diagnoses include: Meningoencephalitis, meningococcemia, upper respiratory infections, urinary tract infections, TTP/ITP, idiopathic vasculitides, toxic shock syndrome, viral gastroenteritis, mononucleosis, and viral gastroenteritis. Drug reaction or serum sickness Kawasaki illness, infective endocarditis, ehrlichiosis, Lyme disease, babesiosis, boutonneuse fever, leptospirosis, and other tick-borne ailments are also the differential diagnosis. Laboratory Results IgM and IgG serologic responses to R. rickettsii, along with a high degree of clinical suspicion, are used to diagnosis the majority of cases with RMSF. Don't put off therapy in anticipation of a cure. Initial Exams (Lab, Imaging) The gold standard in serology is indirect fluorescent antibody (IFA) testing, which is used for specific laboratory diagnoses. - IFA is 94-100 percent sensitive 2 weeks after the start of the illness, but it cannot tell R. rickettsii from other spotted fever-group rickettsii. - It is impossible to distinguish between a single increased IgG titer linked to an acute sickness and earlier infections because of seroprevalence. - It is possible to demonstrate growing IgG or IgM antibody levels by analyzing two serum or plasma samples in succession, which is necessary to confirm an acute infection. - Typically, these samples need to be collected at least two to three weeks apart in order to check for an antibody titer increase of fourfolds or more to confirm the diagnosis. - The best window for testing is 14 to 21 days after the onset of symptoms. Unspecific laboratory examinations - Variable, frequently normal WBC count 60% of children had platelet thrombocytopenia (150,000 cells/L), and 50% of patients have hyponatremia (135 mEq/dL) and increased hepatic transaminases. - Additional symptoms include anemia, a rise in blood urea nitrogen/creatinine, PT/PTT, hyperbilirubinemia, and hypoalbuminemia. - Mononuclear pleocytosis, increased protein, and normal glucose may be seen in CSF. Imaging techniques are rarely beneficial. Other/Diagnostic Procedures A 3-mm punch biopsy can be used to produce a quick direct fluorescent antibody (DFA) test with a sensitivity of 70% and a specificity of 100%. A novel method for diagnosing suspected rickettsial infections during the acute stage of sickness is rickettsial DNA detection utilizing PCR of skin biopsy samples. Enzyme-linked immunosorbent assay (qualitative) Interpretation of Tests Concurrently test serum from the acute and convalescent phases. Early therapy may prevent the production of antibodies. In endemic areas, seropositivity rises with age. The presence of a positive spotted fever group Rickettsia antibody does not always indicate an acute infection. First-line management medication For both adults and children, doxycycline is the drug of choice. Without prompt antibiotic treatment, rickettsial infections have a high rate of morbidity and mortality (20–30%). Other antibiotics have significantly lower efficacy. Doxycycline 100 mg PO or IV every 12 hours until 3 days after the fever goes away in adults and children over the age of 18 who weigh more than 45 kg. Children under 45 kg: Doxycycline 2.2 mg/kg PO or IV every 12 hours till 3 days after the fever goes away. In cases of pregnancy, the first-line treatment is Doxycycline 100 mg PO or IV every 12 hours until 3 days after the fever has subsided. The second-line treatment is chloramphenicol 50 to 75 mg/kg IV divided into 4 doses every day for 7 days. Despite its paucity, the available research indicates that there is no elevated risk of teratogenicity. Fever normally goes down within 24 to 48 hours with early treatment; longer if patient is extremely unwell. Total course of treatment is typically 5 to 7 days, at a minimum, and may be longer if severe or complicated condition. If the patient is promptly treated and doesn't respond to doxycycline within 48 hours, think about a different diagnosis. There is no evidence of RMSF doxycycline resistance. Negative outcomes could include the following: - dyspepsia. With food and water, take your medication. Avoid dairy, iron, and antacids as these may inhibit the absorption of medications. - There could be photosensitivity. Use sunscreen and limit your exposure to the sun. - Children under the age of 8 have no risk of dental discoloration. Doxycycline is contraindicated in cases of severe allergy; in cases of life-threatening illness, fast desensitization may be an option. Next Line The alternate treatment for RMSF is chloramphenicol, which has unfavorable hematologic consequences (such as aplastic anemia) and a higher case death rate. Pregnant women's issues Despite the potential danger to fetal bones or teeth, along with maternal hepatotoxicity and pancreatitis, doxycycline is recommended for this life-threatening illness in pregnancy if suspicion is high. Chloramphenicol may be considered, but it should be avoided in the third trimester due to the risk for gray baby syndrome. Short-term doxycycline is safe with nursing. Referral If a patient has a severe doxycycline allergy, consider having them contact an immunologist or allergist in addition to an infectious disease specialist. Inform public health authorities about any incidences of RMSF. Further Treatments Patients who have suffered neurologic injury could need extensive physical and cognitive therapy. The nedd for oral antibiotic medication for nausea/vomiting prevention and CNS dysfunction are the admission requirements. - Patients with immune system compromise - particular acute organ failure, failure of oral pain medication and shock patients are also reasons for admission into the ICU. Discharge requirements - Fever resolution - Capability to take oral medication and nourishment Follow-up If close follow-up is possible, patients with mild disease may be treated as outpatients. Patients with moderate to severe illness should be hospitalized. Immunity against infection does not last a lifetime. patient observation Until symptoms go away, check on patients receiving outpatient care every 2 to 3 days. If clinically necessary, repeat CBC, electrolytes, and LFTs DIET If intake is inadequate, think about supplemental nourishment. Modification of Lifestyle General precautions and prevention for tick avoidance while outdoors in endemic areas Prognosis Timely administration of the right antibiotics has a significant impact on prognosis. If treatment is delayed until the fifth day of illness, death may increase by three times. The prognosis is excellent with symptom relief and no sequelae when treated quickly. Children under the age of 10 and people over the age of 70 have a higher risk of morbidity and/or fatality, while patients with G6PD deficiency have a higher chance of developing fulminant RMSF, which can be fatal in as little as five days. Complications include: seizures, a focal neurologic deficit, encephalopathy, most usually characterized by a temporary impairment of level of consciousness, and acute renal failure due to renal damage. Hepatitis, respiratory failure, and congestive heart failure (CHF) Additionally possible symptoms include proximal muscular weakness, personality changes, paresthesias, deafness, secondary thromboses, and tissue necrosis. |
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