Mastitis | Inflammation of the Breast

Mastitis is local painful inflammation of the breast that may or may not be accompanied by infection, flulike symptoms, and abscess formation.

 

CAUSE

_ In lactational mastitis, milk stasis and irritation of the milk ducts due to local immune response to milk proteins

  • Bacterial infection of subcutaneous tissue due to breaks in skin.
  • Most commonly, S. aureus; less common, S. epidermidis, group A beta-hemolytic streptococci, S. pneumoniae, E. coli, Candida albicans, M. tuberculosis.

_ GM results from inflammation with epithelioid histiocytes and multinucleated giant cells and can be caused by etiologies like tuberculosis, sarcoidosis, foreign body reaction, parasitic and mycotic infections, or idiopathic.

_ Neonatal mastitis caused by S. aureus or gram-negative enteric bacteria.

RISK FACTOR

_ Previous mastitis

_ Milk stasis and missed feedings

_ Cracked, fissured, or sore nipples

_ Primiparity and infant attachment difficulties

_ Cleft lip or palate or short frenulum in infant

_ Use of manual breast pump

_ Diabetes

_ Breast implants

_ Nipple piercings

CLINICAL

_ Warmth, redness, tenderness in breast

_ Unilateral or bilateral

_ Malaise, myalgias, fevers, chills

_ Decreased milk output

_ Breast is hard and swollen in a wedgeshaped area

_ In PM, breast mass near nipple with retraction or discharge

_ In GM, enlarged axillary lymph nodes or sinus tract formation

DIFFERENTIAL DIANGOSIS

  • Engorgement, plugged duct
  • Breast abscess
  • Inflammatory or other breast cancer (3% of women diagnosed with breast cancer are lactating)
  • Mastitis as a symptom of hyperprolactinemia or galactorrhea
  • GM can be manifestation of systemic disease (sarcoidosis, Wegener granulomatosis, GCA, polyarteritis nodosa, TB, syphilis)

WORKUP

_ History and clinical exam with thorough breast exam and assessment of axillary nodes and nipple discharge are sufficient for diagnosis

LABORATORY TESTS

  • Simple lactational mastitis requires no milk culture or laboratory studies
  • Obtain midstream sample of milk for culture and sensitivities in refractory mastitis or in MRSA-suspected cases
  • CBC and blood cultures in toxic patients
  • In abscess formation, culture of drainage or aspirate fluid
  • Gram stain and culture indicated in infant mastitis

IMAGING

_ Consider US to evaluate for abscess or mammogram when appropriate to exclude carcinoma

MANAGEMENT

_ Warm compresses, increased fluid intake, good nutrition, and rest

_ NSAIDs and analgesics

_ No history of MRSA

  • Dicloxacillin 250 mg 4x/d for 7 d
  • Cephalexin 500 mg 4x/d for 10-14 d
  • Inpatient: nafcillin or oxacillin 2 g IV q4h
  • Erythromycin may be used in patients allergic to penicillin

_ Suspected MRSA or high-risk penicillin allergy

  • Trimethoprim/sulfamethoxazole 160 mg/ 800 mg 2x/d for 10 to 14 d; should not be used when breastfeeding healthy infants <2 mo or compromised infants.
  • Clindamycin 300 mg 4x/d for 10 to 14 d
  • Inpatient: vancomycin 1 g IV q12h

Fibrocystic Breast Disease (FCD) In Management

Fibrocystic breast disease (FCD) is a “nondisease” that includes nonmalignant breast lesions such as microcystic and macrocystic changes, fibrosis, ductal or lobular hyperplasia, adenosis, apocrine metaplasia, fibroadenoma, papilloma, papillomatosis, and other changes. Atypical ductal or lobular hyperplasia is associated with a moderate increase in breast cancer risk.

CLINICAL 

_ Tender breasts

_ Nodular areas

_ Dominant mass

_ Thickening

_ Nipple discharge

_ Can vary with menstrual cycle

CAUSES

_ Although it is frequently seen and diagnosed, mechanism of development is not understood.

_ Because it is found in the majority of healthy breasts, it is regarded as a nonpathologic process.

_ With hormone replacement therapy, the condition may be carried into menopause

DIFFERENTIAL DIAGNOSIS

IMAGING

_ Mammography and ultrasound studies required

MANAGEMENT

  • Not considered a “disease” and does not require treatment.
  • Surgical intervention diagnostic to eliminate possibility of breast cancer.
  • Periodic physician examination to monitor patients with FCD who have pronounced nodular features.
  • Aspiration for palpable cysts (NOTE: Cysts often recur; repeat aspiration is not always required unless pain is a problem).

_ For Breast Pain

  • Danocrine (Danazol): limited success reported but significant side effect profile of medication
  • Bromocriptine or tamoxifen: used less frequently
  • Limited caffeine intake: not as successful in controlling pain or nodularity as originally suggested

Thyroid Nodule in Management

A thyroid nodule is an abnormality found on physical examination of the thyroid gland; nodules can be benign (70%) or malignant.

CAUSE

_ History of prior head and neck irradiation

_ Family history of pheochromocytoma, carcinoma of the thyroid, and hyperparathyroidism (medullary carcinoma of the thyroid is a component of MEN-II).

CLINICAL 

_ Palpable, firm, and nontender nodule in the thyroid area should prompt suspicion of carcinoma. Signs of metastasis are regional lymphadenopathy and inspiratory stridor.

_ Signs and symptoms of thyrotoxicosis can be found in functioning nodules.

DIFFERENTIAL DIAGNOSIS

_ Thyroid carcinoma

_ Multinodular goiter

_ Thyroglossal duct cyst

_ Epidermoid cyst

_ Laryngocele

_ Nonthyroid neck neoplasm

_ Branchial cleft cyst

WORKUP

_ Thyroid ultrasound

_ Fine-needle aspiration (FNA) biopsy

LABORATORY TESTS

_ Serum TSH should be obtained in all patients with thyroid nodules.

_ Thyroid-stimulating hormone (TSH), T4, and serum thyroglobulin levels should be obtained before thyroidectomy in patients with confirmed thyroid carcinoma on FNA biopsy.

_ Serum calcitonin

MANAGEMENT

_ Evaluation of results of FNA:

_ Normal cells: may repeat biopsy during present evaluation or reevaluate patient after 3 to 6 mo of suppressive therapy (l-thyroxine, prescribed in doses to suppress the TSH level to 0.1-0.5).

  • Failure to regress indicates increased likelihood of malignancy.
  • Reliance on repeat FNA biopsy is preferable to routine surgery for nodules not responding to thyroxine.

_ Indeterminate: use of gene expression classifier profile. If suspicious, perform surgery; if benign, monitor with subsequent repeat FNA and gene expression classifier profile.

_ Malignant cells: surgery.

Sinusitis Inflammation

DEFINITION
Sinusitis is infl ammation of the mucous membranes lining one or more of the paranasal sinuses. The various presentations are as folllows:
● Acute sinusitis: infection lasting less than 30 days, with complete resolution of symptoms
● Subacute infection: lasts from 30 to 90 days, with complete resolution of symptoms
● Recurrent acute infection: episodes of acute infection lasting less than 30 days, with resolution of symptoms, which
recur at intervals of at least 10 days apart
● Chronic sinusitis: infl ammation lasting more than 90 days, with persistent upper respiratory symptoms
● Acute bacterial sinusitis superimposed on chronic sinusitis:
new symptoms that occur in patients with residual symptoms from prior infection(s). With treatment, the new
symptoms resolve but the residual ones do not.
PHYSICAL FINDINGS AND CLINICAL PRESENTATION
● Patients often give a history of a recent upper respiratory illness with some improvement, then a relapse.
● Mucopurulent secretions in the nasal passage
● Purulent nasal and postnasal discharge lasting more than 7 to 10 days
● Facial tightness, pressure, or pain
● Nasal obstruction
● Headache
● Decreased sense of smell
● Purulent pharyngeal secretions, brought up with cough, often worse at night
● Erythema, swelling, and tenderness over the infected sinus in a small proportion of patients
● Diagnosis cannot be excluded by the absence of such findings.
● These fi ndings are not common, and do not correlate with number of positive sinus aspirates.
● Intermittent low-grade fever in about one half of adults with acute bacterial sinusitis
● Toothache is a common complaint when the maxillary sinus is involved.
● Periorbital cellulitis and excessive tearing with ethmoid sinusitis
● Orbital extension of infection: chemosis, proptosis, impaired extraocular movements.
Characteristics of acute sinusitis in children with upper respiratory tract infections:
● Persistence of symptoms
● Cough
● Bad breath
● Symptoms of chronic sinusitis (may or may not be present)
● Nasal or postnasal discharge
● Fever
● Facial pain or pressure
● Headache
● Nosocomial sinusitis is typically seen in patients with nasogastric tubes or nasotracheal intubation.

CAUSE
● Each of the four paranasal sinuses is connected to the nasal cavity by narrow tubes (ostia), 1 to 3 mm in diameter; these drain directly into the nose through the turbinates. The sinuses are lined with a ciliated mucous membrane (mucoperiosteum).
● Acute viral infection
● Infection with the common cold or infl uenza
● Mucosal edema and sinus infl ammation
● Decreased drainage of thick secretions, obstruction of the sinus ostia
● Subsequent entrapment of bacteria
a. Multiplication of bacteria
b. Secondary bacterial infection
 Other predisposing factors
● Tumors
● Polyps
● Foreign bodies
● Congenital choanal atresia
● Other entities that cause obstruction of sinus drainage
● Allergies
● Asthma
● Dental infections lead to maxillary sinusitis.
● Viruses recovered alone or in combination with bacteria (in 16% of cases):
● Rhinovirus
● Coronavirus
● Adenovirus
● Parainfluenza virus
● Respiratory syncytial virus
● The principal bacterial pathogens in sinusitis are Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis.
● In the remainder of cases, fi ndings include Streptococcus pyogenes, Staphylococcus aureus, alpha-hemolytic streptococci, and mixed anaerobic infections (Peptostreptococcus, Fusobacterium, Bacteroides, Prevotella).

Infection is polymicrobial in about one third of cases.
● Anaerobic infections seen more often in cases of chronic sinusitis and in cases associated with dental infection; anaerobes are unlikely pathogens in sinusitis in children.
● Fungal pathogens are isolated with increasing frequency in immunocompromised patients but remain uncommon
pathogens in the paranasal sinuses. Fungal pathogens include Aspergillus, Pseudallescheria, Sporothrix, phaeohyphomycoses, Zygomycetes.
● Nosocomial infections occur in patients with nasogastric tubes, nasotracheal intubation, cystic fi brosis, or those who are immunocompromised.
● S. aureus
● Pseudomonas aeruginosa
● Klebsiella pneumoniae
● Enterobacter spp.
● Proteus mirabilis
Organisms typically isolated in chronic sinusitis:
● S. aureus
● S. pneumoniae
● H. infl uenzae
● P. aeruginosa
● Anaerobes

DIFFERENTIAL DIAGNOSIS
● Migraine headache
● Cluster headache
● Dental infection
● Trigeminal neuralgia
WORKUP
● Water’s projection: sinus radiograph
● CT scan
● Much more sensitive than plain radiographs in detecting acute changes and disease in the sinuses
● Recommended for patients requiring surgical intervention, including sinus aspiration; it is a useful adjunct to
guide therapy.
● Transillumination
● Used for diagnosis of frontal and maxillary sinusitis
● Place transilluminator in the mouth or against cheek to assess maxillary sinuses, and under the medial aspect of the supraorbital ridge to assess frontal sinuses.
● Absence of light transmission indicates that sinus is filled with fluid.
● Dullness (decreased light transmission) is less helpful in diagnosing infection.
● Endoscopy
● Used to visualize secretions coming from the ostia of infected sinuses
● Culture collection via endoscopy often contaminated by nasal flora; not nearly as good as sinus puncture
● Sinus puncture
● Gold standard for collecting sinus cultures
● Generally reserved for treatment failures, suspected intracranial extension, nosocomial sinusitis.
TREATMENT
Nonpharmacologic therapy
● Sinus drainage
● Nasal vasoconstrictors, such as phenylephrine nose drops, 0.25% or 0.5%

● Topical decongestants should not be used for more than a few days because of the risk of rebound congestion.
● Systemic decongestants
● Nasal or systemic corticosteroids, such as nasal beclomethasone, short-course oral prednisone
● Nasal irrigation, with hypertonic or normal saline (saline may act as a mild vasoconstrictor of nasal blood fl ow)
● Use of antihistamines has no proved benefi t, and the drying effect on the mucous membranes may cause crusting,
which blocks the ostia, thus interfering with sinus drainage.
● Analgesics, antipyretics.
Antimicrobial therapy
● Most cases of acute sinusitis have a viral cause and will resolve within 2 weeks without antibiotics.
● Current treatment recommendations favor symptomatic treatment for those with mild symptoms.
● Antibiotics should be reserved for those with moderate to severe symptoms who meet the criteria for diagnosis of
bacterial sinusitis.

● Antibiotic therapy is usually empirical, targeting the common pathogens.
● First-line antibiotics include amoxicillin, TMP-SMZ.
● Second-line antibiotics include clarithromycin, azithromycin, amoxicillin-clavulanate, cefuroxime axetil, loracarbef, ciprofloxacin, levofloxacin.
● For patients with uncomplicated acute sinusitis, the less expensive first-line agents appear to be as effective as the
costlier second-line agents.

Surgery
● Surgical drainage indicated
● If intracranial or orbital complications suspected
● For many cases of frontal and sphenoid sinusitis
● For chronic sinusitis recalcitrant to medical therapy
● Surgical débridement imperative for treatment of fungal sinusitis

Gastritis Treatment

INTRODUCTION
Description: Gastritis is an inflammatory condition affecting the stomach lining that results in acute or chronic
indigestion, bloating, “gas,” and heartburn. Prevalence: Common. Predominant Age: Any.
Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS
Causes: Generalized infl ammation of the stomach lining, which, in some cases, may be infectious (Helicobacter
pylori). Risk Factors: Cigarette smoking, alcohol abuse, some medications (nonsteroidal anti-inflammatory drugs
[NSAIDs]), bile reflux, radiation.

CLINICAL CHARACTERISTICS
Signs and Symptoms
• Nausea, vomiting, dyspepsia, heartburn, and “gas” (symptoms are most common after eating large meals,
consuming certain foods)
• Upper abdominal pain or tenderness
• Hiccups
DIAGNOSTIC APPROACH
Differential Diagnosis
• Gastrointestinal reflux
• Ulcer disease (gastric or duodenal)
• Esophageal cancer
• Linitis plastica
Associated Conditions: Bleeding, dysphagia, and gastric or duodenal ulcer.
Workup and Evaluation
Laboratory: No evaluation indicated.
Imaging: No imaging indicated.
Special Tests: Gastroscopy (with or without biopsy) establishes the diagnosis but most often is not necessary.
Diagnostic Procedures: History and physical examination (suspicious), gastroscopy (diagnostic).

MANAGEMENT AND THERAPY
Nonpharmacologic
General Measures: Dietary changes, elevation of the head of the bed, smoking cessation, alcohol in moderation
only, antacids. (Antacids that coat [liquids] and those that tend to fl oat on the surface of the stomach
contents, such as Gaviscon, give better heartburn relief than other agents.)
Specific Measures: Eliminate medications that contribute to reduced esophageal pressure, such as diazepam and calcium channel blockers, or that may damage the esophagus (nonsteroidal anti-infl ammatory drugs). Use
acid-blocking therapy.
Diet: No specifi c dietary changes indicated.
Activity: No restriction.
Patient Education: Reassurance, diet counseling, behavior modification.

Drug(s) of Choice
Antacids.
Histamine H2 antagonists (cimetidine 800 mg two times daily, ranitidine 400 mg four times daily, famotidine
20 mg two times daily, or nizatidine 150 mg two times daily).
Hydrogen potassium pump blocker (omeprazole 20 to 40 mg daily for 4 to 8 weeks, esomeprazole 20 to 40 mg
daily for 4 to 8 weeks, or pantoprazole 40 mg daily for 8 weeks). Misoprostol (Cytotec, 100 to 200 microg PO
four times daily) if mucosal injury is documented or suspected.
Contraindications: Known or suspected hypersensitivity. Misoprostol is contraindicated during pregnancy and
lactation.
Precautions: If bismuth is prescribed, warn the patient about black stools. Because of a lack of long-term followup,
hydrogen pump inhibitors may be taken for only 8 to 12 weeks.
Interactions: Multiple drug interactions are possible with agents such as cimetidine; check full prescribing
information.

Alternative Drugs
In patients with H. pylori infection, a combination of bismuth (Pepto-Bismol) and an antibiotic (metronidazole
250 mg every 6 hours, tetracycline 500 every 6 hours, or amoxicillin 500 mg every 8 hours) has been recommended for 2 weeks. A 4-week treatment with clarithromycin (Bixin) and either omeprazole (Prilosec) or ranitidine bismuth citrate (Tritec) may also be used.
FOLLOW-UP
• Patient Monitoring: Normal health maintenance. If significant gastric erosion is documented, repeat gastroscopy
after 6 weeks is often recommended.
• Prevention/Avoidance: Reduction of modifi able risk factors (e.g., smoking).
• Possible Complications: Chronic pain, ulcer formation, and perforation.
• Expected Outcome: Generally good symptomatic relief, but long-term therapy is often required.

Varicose

DEFINITION
Veins in the leg are soft, thin-walled tubes that return blood back to the heart. This is accomplished
by the presence of one-way valves and the action of the calf pump. Superficial venous insufficiency develops when venous return is impaired by valvular incompetence, obstruction, or calf muscle pump failure.
Varicose veins, the most common clinical manifestation of chronic venous disease, are bulging (>3 mm in diameter), tortuous conduits. Reticular veins, often called “feeder veins,” are bluish subdermal veins about 1 to 3 mm in diameter that give rise to telangiectasia. Spider veins or telangiectasias are very small (≤1 mm in diameter) thread veins found commonly in clusters on the surface of the skin.

EPIDEMIOLOGY
PREVALENCE: One large U.S. cohort study found the biannual incidence of varicose veins was 3% in women and 2% in men. The prevalence of varicose veins in Western populations was estimated in one study to be
about 25% to 30% in women and 10% to 20% in men.
RISK FACTORS
Gender: female
Genetics: family history of varicose veins Increasing age ,Multiple pregnancies.

CLINICAL PRESENTATION
• Chronic vein disease is the result of the introduction of high pressures into a normal low-pressure superficial venous system.
• This increased pressure or venous hypertension causes superficial veins to distend to such a degree that vein valves fail to close, causing reflux and pooling of blood in surface veins.
• Manifested clinically by two syndromes:
1. Junctional: failure of the terminal valve at the intersection between the saphenous vein trunks and the deep system. If the great saphenous vein is involved, large varicose veins are found mainly above medial knee or calf. When the small saphenous vein is involved, large varicose  veins are found in posterior knee or calf area. If the anterior accessory of great saphenous vein is involved, large varicose veins are found mainly in anterior or lateral thigh.
2. Perforator: failure of valves located in perforating vein. Large varicose veins are found most commonly in medial calf and proximal thigh region.
CLASSIFICATION
Chronic venous disease can now be classified using the Clinical-Etiology-Anatomy- Pathophysiology (CEAP) criteria to allow a precise description of the type of venous disease being discussed and provide an orderly framework for decision making.

ETIOLOGY
• The underlying etiology of varicose veins remains uncertain.
• Important structural changes that occur: failure of vein valve function and vein wall dilation from fragmentation of the muscle layer.
COMPLICATIONS
• Superficial venous thrombophlebitis (SVT): a very common disorder with an incidence of 125,000 new cases per year in the U.S. The most frequent predisposing risk factors are varicose veins. The clinical findings include
the presence of erythema, tenderness, and a palpable cord. Pain, increased warmth, and swelling are also present. Diagnosis is made by ultrasonography, which is useful to identify associated deep vein thrombosis that can
occur in approximately 15% of patients. The location of the SVT determines the course of treatment; if the proximal great saphenous vein (GSV) is involved, a 1-mo course of sion stockings has been found to be more effective than vein ligation. If SVT involves branch varicosities, treatment is usually symptomatic (control of pain).
• Bleeding is a more common complication than traditionally suspected. It is associated with thin-walled ectatic veins known as “blue blebs” that are found predominantly in the medial lower calf and ankle region.                               The best emergency treatment consists of pressure wrapping and not suture ligation, which results in delayed healing of the bleeding site. Sclerotherapy of these veins is the definitive treatment to prevent further bleeding.

DIFFERENTIAL DIAGNOSIS
Other conditions that cause leg pain:
• Stress fracture
• Arthritis hip/knee joint
• Gout
• Degenerative disk disease of lower back
• Intermittent claudication secondary to peripheral arterial disease (PAD)
• Medications such as allopurinol and statins Other conditions that cause leg swelling:
• Cellulitis
• Soft tissue injury to leg/ankle/foot

TREATMENT
CONSERVATIVE THERAPY
• Aerobic exercise regularly for 30 min a day.
• Elevate legs above heart level to reduce swelling.

• Flex ankles frequently at work and during air travel or long car travel.
• Maintain proper weight.
• Graduated compression stockings (below knee) to alleviate symptoms in patients who are not candidates or do not desire to undergo treatment of their varicose veins.
SCLEROTHERAPY
• Small- to medium-sized varicose veins such as spider veins and reticular varices in the absence of reflux in saphenous trunks are best treated with liquid sclerotherapy.
• The three principal sclerosants used in the U.S. are hypertonic saline, sodium tetradecylsulfate, and the newly FDA-approved solution, polidocanol.
• These agents are injected into vessels using 27-gauge or 30-gauge needles at concentrations of 23.4%, 0.1%, or 0.5%, respectively, causing injury to the endothelium with the resultant disappearance of the vein over period of time (usually 8-12 wk).
AMBULATORY PHLEBECTOMY
• A procedure in which large varicose vein branches are removed with special hook instruments through a small puncture— incisions are made with an 18-gauge needle or No. 11 blade
• Performed safely under local anesthesia in an office setting and offers excellent cosmetic results and relief of symptoms
• Most commonly performed in conjunction with endovenous ablation procedures

ENDOVENOUS ABLATION
• Ablation of diseased saphenous vein trunks, large incompetent tributaries, or perforating veins can be achieved by using:
1. Radiofrequency energy
2. Laser energy
3. Ultrasound-guided foam sclerotherapy.
• The first two accomplish thermal injury to the vein in situ via an intraluminal catheter or bare-tipped laser wire. Chemical ablation uses a solution (polidocanol or sodium tetradecyl sulfate) that is injected directly into the
vein in the form of foam.
• Endovenous ablation can be performed in an office setting using local anesthesia. Patients can return to their normal daily activities immediately.
• The efficacy of these endovenous ablation procedures has been borne out by numerous published reports with occlusion rates over 95% and reflux free rates over 5-yr follow-up of 86%. A recent trial comparing ultrasoundguided
foam sclerotherapy and endovenous laser ablation revealed that quality of life measures were generally similar among the study groups, with the exception of a slightly worse disease-specific quality of life in the foam group than in the surgery group. Both treatments had similar efficacy, but complications were less frequent after laser treatment
and ablation rates were lower after foam treatment.

Diabetic Foot Ulcer Management

DEFINITION
Diabetic foot infections (DFIs) are a common and potentially serious problem in persons with diabetes. They usually arise from either a skin ulceration that occurs secondarily to peripheral neuropathy or in a wound caused by some form of trauma. The infection usually involves one or more bacteria and can spread to contiguous tissues including bone, causing an osteomyelitis.

Diabetes mellitus (DM), a common complex metabolic disorder characterized by hyperglycemia, affects over 18 million people in the United States. The skin is one of many organ systems affected, especially the skin of the leg and foot. Microvascular disease may result in a decreased cutaneous blood fl ow; peripheral sensory neuropathy may render the skin susceptible toinjury and may blunt healing; and hyperglycemia predisposes the extremity to an increased occurrence of bacterial and fungal infections.

Associated complications in the lower limb include Charcot joint (progressive destructive arthropathy caused by
neuropathy), ulceration, infection, gangrene, and amputation. DM accounts for most nontraumatic foot and lower leg amputations, which total more than 80,000 per year.

Atherosclerosis can affect not only the coronary and cerebral vasculature but also the arteries that supply the kidneys, intestines, and lower limbs. The resulting arterial stenosis (narrowing) or occlusion in the leg leads to peripheral vascular disease (PVD), a disorder largely associated with increasing age. PVD produces symptoms of claudication, which should be a warning sign of atherosclerosis elsewhere that may produce myocardial infarction and stroke.

RISK FACTORS:
• Diabetes greater than 10 years
• Poor glucose control
• Peripheral neuropathy: altered protective sensation and altered pain response
• Diabetic angiopathy: atherosclerotic obstruction of larger vessels leading to peripheral vascular disease
• Evidence of increased local pressure: callus or erythema.

DIFFERENTIAL DIAGNOSIS
Other inflammatory conditions that can mimic diabetic foot infections include:
• Crystal-associated arthritis such as gout
• Trauma
• Acute Charcot arthropathy from long-standing diabetes
• Venous stasis ulcers
• Deep vein thrombosis

ACUTE GENERAL TREATMENT
WOUND MANAGEMENT:
• Debridement of callus and necrotic tissues by wound care specialist or surgeon and at times may require multiple debridements.
• Wound dressing: to absorb exudates and promote healing. Many products are available but none has been proven superior and include:
1. Enzymes
2. Gels
3. Hydrocolloids
4. Antiseptics containing iodine or silver salts
5. Honey
• Relieve pressure on the foot: casts or special shoes.
• Amputation or revascularization procedures such as angioplasty or bypass grafting may be necessary.

Asthma Attack

Introduction
Asthma is a syndrome with a chronic but variable clinical course and presentation. Its main features are (1)
reversible airflow obstruction, (2) nonspecific airways hyper-reactivity, and (3) airways inflammation. The nonspecific nature of the hyper-reactivity is perhaps a reflection of airway inflammation. Symptoms are triggered
by nonallergic stimuli such as smoke and strong odors and quantifi ed by sensitivity to inhalational challenge
to nonallergic stimuli such as histamine. Airway hyperreactivity predisposes patients to symptoms in a variety
of environments.

Both children and adults develop asthma. The remission rate in adults is 10% to 15% but is more than 50%
in children. Despite advances in the understanding of asthma and better medications, asthma morbidity and
mortality have increased. During the past 110 years, our understanding of asthma has changed greatly. It was
long considered a disease of “twitchy” airways and a minor ailment that, according to Osler, allowed the patient
to “pant into old age.” Now, asthma is considered a disease of chronic fl uctuating airways infl ammation with
a lethal potential of 5000 deaths annually in the United States. It is a major public health problem that results
in 1.8 million emergency room visits per year, with about 10% of patients requiring hospitalization at a cost
of $12 billion annually in the United States.

Etiology and Pathogenesis
Asthma manifests as inflammation in the lower airways. Over time, structural changes in the airway called remodeling result (i.e., muscle hypertrophy and thickening of the basement membrane) . Acute asthma exacerbations cause airway muscle contraction, edema and sloughing of the airway mucosa, and the accumulation of mucus, cellular debris, and exudative secretions in the airway lumen. These changes degrade airway function, causing respiratory symptoms and even death by suffocation.
There are clinical and epidemiologic links between asthma and immunoglobulin E (IgE). Transcription
factors, such as nuclear factor-KB and members of the signal transduction-activated transcription (STAT) factor
family, act on genes encoding for infl ammatory cytokines, such as interleukins (ILs), and appear to initiate and sustain airway  inflammation. Corticosteroids are the most effective controllers of asthma. They inhibit these
transcription factors and airway infl ammation. Asthma refractory to corticosteroids has been linked to the tumor
necrosis factor axis. However, the newly described subset of natural killer T (NKT) cells, CD1d-restricted NKT
cells, with potent immunoregulatory functions and associated with asthma, are also resistant to modulation by
corticosteroids.

A widely held mechanistic explanation is that inhaled antigen activates mast cells and T helper type 2 (Th2)
lymphocytes, causing mediator release that promotes a persistent eosinophilic airway infl ammation. There is no
clear understanding of which biologic infl uences lead to chronic eosinophilic airway infl ammation and hyperresponsiveness in asthma. Genetic factors (e.g., polymorphism for the IgE receptor, β receptor, matrix
metalloproteinase, and CD14), environmental factors (e.g., excessive hygiene, vaccinations), and triggers (e.g., viral
infection, exposures to tobacco smoke, pollutants, allergens) have all been implicated in the pathogenesis of asthma . Most asthmatic patients are atopic and have IgE-mediated disease, although there is evidence suggesting that intrinsic or nonatopic asthmatic patients may produce local, as opposed to circulating, IgE. Inflammation in atopic asthma can be demonstrated when the patient is challenged with inhaled allergen.

The sensitive patient will show decline in pulmonary function demonstrated by obstruction of airflow with spirom-etry and decrease in the forced expiratory fl ow at 1 second (FEV1) and in the peak expiratory fl ow rate (PEFR). There is an initial decline within about 20 minutes associated with histamine release from mast cells that is stimulated by allergen binding to IgE on the mast cell surface. This immediate reaction is blocked by antihistamines but not by steroids. Classically, a spontaneous recovery occurs, only to be followed by a second, later decline in fl ow rates. Steroid pretreatment inhibits this late phase reaction, which is manifest by the recruitment of inflammatory cells into and around the lower airway.

Management and Treatment Of Acute Appendicitis

Appendectomy 

Acute appendicitis. Interval procedure following management of an appendix mass with IV
antibiotics.

ANATOMY

The appendix arises at the convergence of the taeniae coli on the posteromedial side of the caecum, 2.5 cm below the junction with the terminal ileum. The length varies from 1.2 to 22.0 cm and the appendix can lie in variable positions, retrocaecal (70%), pelvic (20%), subcaecal (2%) and pre- or post-ileal (5%). It has a mesentery, the mesoappendix, in which runs the appendicular artery, a branch of the ileocolic artery. Lymphatics from the appendix
traverse the mesoappendix to drain into ileocaecal nodes.

INVESTIGATIONS

Pre-op: FBC, U&Es, LFT, amylase, CRP and urinalysis (for investigation of abdominal pain). In
females of childbearing age, a pregnancy test should be performed. Antibiotic are started if there are signs of sepsis, otherwise a single prophylactic dose is given at the time of surgery.
Post-op: Antibiotics may be continued if the appendix is inflamed. DVT prophlyaxis.

PROCEDURE
Can be performed laparoscopically or open. Always examine the patient on the table to see if a mass is present.
Access: Lanz (horizontal skin crease) incision, centred on McBurney’s point (2/3 the distance from umbilicus to anterior superior iliac spine), the subcutaneous fat is divided and external oblique aponeurosis exposed. A small slit is made in the direction of the fibres, then extended with scissors. Internal oblique muscle is split along the direction of its fibres by blunt dissection, as is transversus, and the opening is gently enlarged using retractors.
Once the peritoneum is exposed, it is gently picked up with a clip. A second clip is then placed and the first clip repositioned. Palpate to ensure there is no bowel caught between the clips before a small cut is made, and then extended. Identification: The peritoneal cavity is inspected for free fluid or pus. The caecum is identified and the taeniae are followed to find the base of the appendix, freeing it from inflammatory adhesions by gentle blunt dissection. Babcock’s forceps is used to pick up the appendix.
If the appendix is found to be normal (‘lily-white’), it should still be removed, however, the small bowel should be systematically inspected for terminal ileitis, a Meckel’s diverticulum or mesenteric adenitis. In females, the right ovary and tube should be inspected.

Resection: The mesoappendix is clipped and divided after tying off, ensuring haemostasis. A crushing clamp is used to crush the base of the appendix and the base is transfixed or tied before removal. The appendix is sent for histological analysis. Usually the appendix stump is buried using a purse string suture. The cavity should be washed if there has been inflammatory fluid or pus.
Closure: The incision is then closed in layers. A continuous suture of the peritoneum, interrupted sutures to the muscle layers and then continuous sutures to the external oblique (the latter is very important in preventing subsequent hernias) are performed. A subcuticular absorbable suture is usually used for the skin. Local anaesthetic infiltration reduces post-op pain.

Laparoscopic appendicectomy: An alternative technique, which is very useful in women where the diagnosis may be equivocal as it can be both diagnostic and therapeutic. Following capnoperitoneum and port placement, the mesoappendix is divided from the appendix and loop suturing or endostapling across the appendix base before excision and removal through a port.

Diabetes Mellitus (DM) In Management

DEFINITION
Diabetes mellitus (DM) refers to a syndrome of hyperglycemia resulting from many different causes. It can be classified into type 1 (formerly insulin-dependent diabetes mellitus [IDDM]) and type 2 (formerly non–insulin-dependent diabetes mellitus [NIDDM]). Because insulin-dependent and non–insulindependent refer to the stage at diagnosis, when a type 2 diabetic needs insulin, he or she remains classifi ed as type 2 and does not revert to type 1.
The American Diabetes Association (ADA) defi nes DM as (1) a fasting plasma glucose 126 mg/dL, (2) a nonfasting
plasma glucose 200 mg/dL, or (3) glucose 200 mg/dL in the 2-hour sample in an oral glucose tolerance test (OGTT). Furthermore, a value of 100 mg/dL of fasting blood sugar is the upper limit of normal for glucose. A fasting glucose between 100 and 126 mg/dL is classifi ed as impaired fasting glucose (IFG).

CAUSE
Idiopathic diabetes
TYPE 1 DIABETES MELLITUS
● Hereditary factors
1. Islet cell antibodies (found in 90% of patients within the first year of diagnosis)
2. Higher incidence of HLA types DR3, DR4 3. 50% concordance in identical twins
● Environmental factors: viral infection (possibly coxsackie virus, mumps virus)
TYPE 2 DIABETES MELLITUS
● Hereditary factors: 90% concordance in identical twins
● Environmental factor: obesity

Diabetes secondary to other factors
● Hormonal excess: Cushing’s syndrome, acromegaly, glucagonoma, pheochromocytoma
● Drugs: glucocorticoids, diuretics, oral contraceptives
● Insulin receptor unavailability (with or without circulating antibodies)
● Pancreatic disease: pancreatitis, pancreatectomy, hemochromatosis
● Genetic syndromes: hyperlipidemias, myotonic dystrophy, lipoatrophy
● Gestational diabetes

DIFFERENTIAL DIAGNOSIS
● Diabetes insipidus
● Stress hyperglycemia
● Diabetes secondary to hormonal excess, drugs, pancreatic disease
PHYSICAL FINDINGS AND CLINICAL PRESENTATION
● Physical examination varies with the presence of complications and may be normal in early stages.
● Diabetic retinopathy
● Nonproliferative (background diabetic retinopathy)
1. Initially: microaneurysms (Fig. 285–1), capillary dilation, waxy or hard exudates, dot and fl ame hemorrhages , arteriovenous (AV) shunts 2. Advanced stage: microinfarcts with cotton-wool exudates, macular edema
● Proliferative retinopathy: characterized by formation of new vessels , vitreal hemorrhages, fibrous scarring,
and retinal detachment
● Cataracts and glaucoma occur with increased frequency in diabetics.
● Peripheral neuropathy: patients often complain of paresthesias of extremities (feet more than hands); the symptoms are symmetrical, bilateral, and associated with intense burning pain (particularly during the night).
● Mononeuropathies involving cranial nerves III, IV, and VI, intercostal nerves, and femoral nerves are also common.

TREATMENT
● Diet
● Calories
1. The diabetic patient can be started on 15 cal/lb of ideal body weight; this can be increased to 20 cal/lb for an active
person and 25 cal/lb if the patient does heavy physical labor.
2. The calories should be distributed as 50% to 60% carbohydrates, less than 30% fat, with saturated fat limited to less than 10% of total calories, and 15% to 20% protein.
3. The emphasis should be on complex carbohydrates rather than simple and refi ned starches and on polyunsaturated instead of saturated fats in a ratio of 2:1.
● Seven food groups
1. The exchange diet of the ADA includes protein, bread, fruit, milk, and low- and intermediate-carbohydrate vegetables.
2. The name of each exchange is meant to be all-inclusive (e.g., cereal, muffins, spaghetti, potatoes, rice are in the
bread group; meats, fish, eggs, cheese, peanut butter are in the protein group).
3. The glycemic index compares the rise in blood sugar after the ingestion of simple sugars and complex carbohydrates with the rise that occurs after the absorption of glucose.
Equal amounts of starches do not produce the same increase in plasma glucose (pasta equal in calories to a baked
potato causes less of an increase than the potato). Thus, it is helpful to know the glycemic index of a particular food
product.
4. Fiber: insoluble fi ber (bran, celery) and soluble globular fiber (pectin in fruit) delay glucose absorption and attenuate the postprandial serum glucose peak. They also appear to lower the elevated triglyceride level often present in uncontrolled diabetics. A diet high in fiber should be emphasized (20 to 35 g/day of soluble and insoluble fiber).