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Clinical disease: Inhalation anthrax: In addition to pulmonary symptoms patients more frequently have nausea generic clozapine 50 mg overnight delivery depression comix, vomiting buy generic clozapine 50 mg on-line mood disorder risk factors, pallor or cyanosis buy 25 mg clozapine fast delivery depression anxiety test online, diaphoresis buy clozapine 50 mg low cost depression men, confusion, tachycardia >110 beats/min, temperature >100. Hemorrhagic meningoencephalitis was present in 50% of autopsy deaths after the accidental release of anthrax in Sverdlovsk. Hemorrhagic Meningoencephalitis Neurologic spread of infection may occur with inhalation disease, cutaneous disease, or gastrointestinal disease. Patients also develop cerebral edema, intracerebral hemorrhages, vasculitis, and subarachnoid hemorrhages. Cutaneous Anthrax (Also Known as Malignant Pustule) This is the most common form of anthrax. A painless black eschar with local edema is seen, which eventually dries and falls off in one to two weeks. Patients may succumb from necrotizing enterocolitis with hemorrhagic ascitic fluid. Differential diagnosis: Cutaneous anthrax: plague, tularemia, scrub typhus, rickettisal spotted fevers, rat-bite fever, ecthyma gangrenosum, arachnid bites, and vasculitis. Treatment: Ciprofloxacin or doxycycline for the initial intravenous therapy until susceptibility is reported. Prophylaxis is necessary for those exposed to the spores (usually 480 Cleri et al. Delay in initiating antibiotics in patients with pulmonary disease resulted in a 40% to 75% mortality. Rabies (119–126) Virology: Rabies virus is a negative-stranded enveloped lyssavirus (lyssavirus type 1). Classical rabies virus is the only naturally occurring lyssavirus in the western hemisphere. The virus is stable between pH 3 and 11 and will survive for years at À708C or when freeze-dried and stored at 08Cto48C. Risk of transmission: Rabies is commonly transmitted by a bite or lick of a rabid animal. Corneal transplants have been responsible for a number of human-to-human infections. Rabies virus may be transmitted from human to human as the virus has been isolated from saliva, respiratory secretions, sputum, nasal swabs, pharyngeal swabs, eye swabs, tears, cerebrospinal fluid, urine, blood, and serum. Anecdotal reports of rabies transmission by lactation, kissing, a bite, intercourse, providing health care, and transplacental (human) have been reported. Bait laced with attenuated rabies virus has transmitted the infection to animals and the consumption of dying or dead vampire bats has transmitted the infection to foxes and skunks. Cryptogenic rabies (no evidence or history of an animal bite) represents the largest group of human rabies cases in the United States. Two strains of rabies virus associated with two species of bats rarely found among humans were responsible for the majority of cases. These two strains of rabies virus (i) replicate at lower temperatures, (ii) easily infect skin because of their ability to infect fibroblasts and epithelial cells, (iii) grow in higher titers in epithelial and muscle tissue as compared to dog or coyote street rabies virus, and (iv) have changes in the antigenic sites that increases infectivity. Incubation period: The average incubation period (Stage I) is one to two months (range: 4 days to 19 years). Half the patients have fever and chills and in some patients, gastrointes- tinal symptoms predominate including nausea, vomiting, diarrhea, and abdominal pain. At the bite site or proximally along the nerve radiation, there is itching, pain, or paresthesia. Myoedema (mounding of a part of the muscle when hit with the reflex hammer) may be demonstrated. Patients are agitated, hyperactive, waxing and waning alertness, bizarre behavior, hallucinations, aggression, with intermittent lucid periods. There is piloerection, excessive salivation, sweating, priapism, repeated ejaculations, and neurogenic pulmonary edema. Hydrophobia begins with difficulty swallowing liquids resulting in pharyngeal and laryngeal spasms and aspiration. Symptomatic dumb or paralytic rabies patients have a longer average survival (13 days). Patients present with weakness or paralysis in a single limb or may present with quadriplegia. There is pain and fasciculation in the affected muscle groups, and sensory abnormalities in some patients. Some patients survive as long as a month without respiratory support but eventually die with paralysis of respiratory and swallowing muscles. Bioterrorism Infections in Critical Care 481 Recovery or Death (Stage V) On average, death occurs 18 days after the onset of symptoms. Patients cared for in intensive care units have survived from 25 days to months with respiratory support. Death in these patients is often from myocarditis with arrhythmia or congestive heart failure. Differential diagnosis: Other causes of viral encephalitis, tetanus (when opisthotonos is present), acute inflammatory polyneuropathy, transverse myelitis, and poliomyelitis. When there is a prolonged incubation period, clinical disease may suggest progressive multifocal leukoencephalopathy. Treatment in an intensive care unit should be considered if (i) the patient received rabies vaccine before the onset of symptoms, (ii) the patient presents at a very early stage of disease (i. Some authors disagree about limiting therapy to cases strictly in the earliest stages (122). Contacts should be traced to at least one week prior to the onset of neurologic symtpoms in order to provide them with prophylaxis. Postexposure prophylaxis: People previously vaccinated against rabies within two years and who have evidence of immunity: 1. In the absence of documented immunity, the full schedule of postexposure prophylaxis is indicated. She was discharged alert, but with choreoathetosis, dysarthria, and unsteady gait (123). Ketamine-induced coma and ribavirn therapy has failed in other patients (121,124). Based upon this finding, investigators monitored flow velocities, and resistive and pulsatility indices of the middle cerebral arteries by transcranial Doppler. What is simultaneously considered after the initial recognition that the patient may be a victim of bioterrorism includes the most likely diagnosis and differential diagnosis, the broadest emergent treatment, identification and prophylaxis of contacts where indicated, and isolation and safety precautions. Other scenarios include: (i) the patient being infected with two or more agents, especially with differing incubation periods; (ii) additional victims presenting similarly but infected with a different pathogen or pathogens as a result of a second simultaneous attack; (iii) a second attack at a later time with the same or different agents; and (iv) genetically altered agents that renders them more resistant to treatment and/or more difficult to identify. An even more sinister possibility is that the hospital (building, buildings, or campus) becomes one of the primary or secondary targets. Clinicians confronted with the first victims must put themselves into the mind of the enemy. Diagnostic, therapeutic, and infection control decisions must be quickly implemented, and often based upon inadequate data. They should take into account the possibility of a second pathogen in the same patient or different pathogens in subsequent patients early in the outbreak before there is an alteration in the initial and usually most stringent isolation precautions. Epidemiologic, clinical, laboratory, and historical data on the first patients will often be the key to identifying the pathogen(s), means of distribution, and the culprits responsible. Again, the terrorists may be among the first and most critically ill patients presenting to the intensive care unit. Cannon to right of them, Cannon to left of them, Cannon behind them Volley’d and thunder’d; Storm’d at with shot and shell, While horse and hero fell, They that had fought so well Came thro’ the jaws of Death Back from the mouth of Hell, All that was left of them, Left of six hundred.
Identiﬁcation—A sexually transmitted bacterial disease limited to columnar and transitional epithelium order 100mg clozapine overnight delivery mood disorder due to medical condition, which differs in males and females in course buy clozapine 100mg free shipping depression nutrition, severity and ease of recognition discount clozapine 100 mg free shipping depression weight gain. In males cheap 25mg clozapine with mastercard bipolar depression 40, gonococcal infection presents as an acute purulent discharge from the anterior urethra with dysuria within 2–7 days after exposure. The Gram stain is highly sensitive and speciﬁc for documenting urethritis and the presence of gonococcal infection in symptomatic males. In females infection is followed by the development of mucopurulent cervicitis, often asymptomatic, although some women have abnormal vaginal discharge and vaginal bleeding after intercourse. In about 20% there is also uterine invasion, often at the ﬁrst, second or later menstrual period, with symptoms of endometritis, salpingitis or pelvic peritonitis and subsequent risk of infertility and ectopic pregnancy. Prepubescent girls may develop gonococcal vulvovaginitis through direct genital contact with exudate from infected people during sexual abuse. In females and homosexual males, pharyngeal and anorectal infections are common and, while usually asymptomatic, may cause pruritus, tenes- mus and discharge. Conjunctivitis occurs in newborns and rarely in adults, with resultant blindness if not rapidly and adequately treated. Arthritis can produce permanent joint damage if appropriate antibiotherapy is delayed. Diagnosis is made by Gram stain of discharges, bacteriological culture on selective media (e. Typical Gram-negative intracellular diplococci can be considered diagnostic in male urethral smears; they are nearly diagnostic when seen in cervical smears (speciﬁcity 90%–97%). Cultures on selective media, plus presumptive identiﬁcation based on both macro- scopic and microscopic examination and biochemical testing, are sensitive and speciﬁc, as are nucleic acid detection tests. In cases with potential legal implications, specimens should be cultured and isolates conﬁrmed as N. Occurrence—Worldwide, the disease affects both men and women, especially sexually active adolescents and younger adults. In most industrialized countries, incidence has decreased during the past 20-odd years, although it appears to have increased again since 1995; the rise has been greatest in the younger age groups. New infections tend to be concentrated in population subgroups at increased risk, such as men who have sex with men and ethnic minorities. Mode of transmission—Contact with exudates from mucous membranes of infected people, almost always as a result of sexual activity. Humoral and secretory antibodies have been demonstrated, but gonococcal strains are antigeni- cally heterogeneous and reinfection is common. Women using an intra- uterine contraceptive device have higher risks of gonococcal salpingitis during the ﬁrst 3 months after insertion; some people deﬁcient in complement components are uniquely susceptible to bacteraemia. Preventive measures: 1) Same as for syphilis (see Syphilis, 9A), except for measures that apply speciﬁcally to gonorrhoea, i. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Case report is required in many countries, Class 2 (see Reporting). Effective antibiotics in adequate dosage promptly render discharges noninfectious. Patients should refrain from sexual intercourse until antimicrobial therapy is completed, and, to avoid reinfection, abstain from sex with previous sexual partners until these have been treated. With uncooperative patients, trained interviewers obtain the best results, but clinicians can motivate most patients to help arrange treat- ment for their partners. Sexual contacts of cases should be examined, tested and treated if their last sexual contact with the case was within 60 days before the onset of symptoms or diagnosis in the case. Even outside these time-limits the most recent sexual partner should be examined, tested and treated. Providing patients under treatment for gonorrhoea with a treatment effective against genital chlamydial infection is recommended routinely because chlamydial infection is com- mon among patients diagnosed with gonorrhoea. This will also cure incubating syphilis and may inhibit emergence of antimicrobial-resistant gonococci. Gonococcal infections of the pharynx are more difﬁcult to eliminate than infections of the urethra, cervix or rectum. Resistance of the gonococcus to common antimicrobials is due to the widespread presence of plasmids that carry genes for resistance. Treatment failure following any of the antigonococcal regimens listed above is rare, and routine culture as a test of cure is unnecessary. If symptoms persist, reinfection is most likely, but specimens should be obtained for culture and antimicrobial susceptibility testing. Retesting of high-risk patients after 1–2 months is advisable to detect late asymp- tomatic reinfections. Epidemic measures: Intensify routine procedures, especially treatment of contacts on epidemiological grounds. Identiﬁcation—Acute redness and swelling of conjunctiva in one or both eyes, with mucopurulent or purulent discharge in which gono- cocci are identiﬁable by microscopic and culture methods. Corneal ulcer, perforation and blindness may occur if speciﬁc treatment is not given promptly. Gonococcal ophthalmia neonatorum is only one of several acute inﬂammatory conditions of the eye or the conjunctiva occurring within the ﬁrst 3 weeks of life, collectively known as ophthalmia neonatorum. The commonest infectious cause is Chlamydia trachomatis, which produces inclusion conjunctivitis that tends to be less acute than gono- coccal conjunctivitis and usually appears 5–14 days after birth (see Conjunctivitis, chlamydial). Any purulent neonatal conjunctivitis should be considered gonococcal until proven otherwise. Occurrence—Varies widely according to prevalence of maternal infections and availability of measures to prevent eye infections in the newborn at delivery; it is infrequent where infant eye prophylaxis is adequate. Period of communicability—While discharge persists if untreat- ed; for 24 hours following initiation of speciﬁc treatment. Preventive measures: 1) Prevent maternal infection (see section I, 9A and Syphilis, 9A). Diagnose gonorrhoea in pregnant women and treat the woman and her sexual partners. Routine culture of the cervix and rectum for gonococci should be considered prenatally, especially in the third trimester where infection is prevalent. A study carried out in Kenya found that the incidence of ophthalmia neonatorum in infants treated with a 2. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Case report is required in many countries, Class 2 (see Reporting). Identiﬁcation—A chronic and progressively destructive, but poorly communicable bacterial disease of the skin and mucous mem- branes of the external genitalia, inguinal and anal regions. One or more indurated nodules or papules lead to a slowly spreading, nontender, exuberant, granulomatous, ulcerative or cicatricial lesions. The lesions are characteristically nonfriable beefy red granulomas that extend peripherally with characteristic rolled edges and eventually form ﬁbrous tissue. Lesions occur most commonly in warm, moist surfaces such as the folds between the thighs, the perianal area, the scrotum, or the vulvar labia and vagina. The genitalia are involved in close to 90% of cases, the inguinal region in close to 10%, the anal region in 5%–10% and distant sites in 1%–5%. If neglected, the process may result in extensive destruction of genital organs and spread by autoinoculation to other parts of the body. Laboratory diagnosis is based on demonstration of intracytoplasmic rod shaped organisms (Donovan bodies) in Wright- or Giemsa-stained smears of granulation tissue or on histological examination of biopsy specimens; the presence of large infected mononuclear cells ﬁlled with deeply staining Donovan bodies is pathognomonic. Haemophi- lus ducreyi should be excluded by culture on appropriate selective media. Infectious agent—Klebsiella granulomatis (Donovania granulo- matis, Calymmatobacterium granulomatis), a Gram-negative bacillus, is the presumed causal agent; this is not certain.
Possibly clozapine 100 mg for sale clinical depression definition dsm, it is too faint; it must multiply and create a loud chorus before you can hear it cheap clozapine 50mg otc anxiety rash symptoms. Then the tape eggs hatch into the cysticercus stage clozapine 25 mg overnight delivery anxiety 6 letters, which promptly gets to the liver clozapine 100 mg recurrent depression definition. If you can do both, you may be able to see which organ allows the virus to replicate after it emerges. They are on your kitchen sponge, and in any food or dishes that stand uncovered anywhere in the home. Muscles that are diseased will take in the newcomer and allow it to survive add- ing to the parasites and pollutants already there! You will need to search sev- eral times during the day to find it in your white blood cells. You can find out by waiting until a time when you have a tapeworm stage or mite and no Adenovirus. And minutes later you may feel a stuffy nose, a slight congestion developing, a certain head feeling that is different. Yes, this “baby cold” will develop into a full blown cold if, but only if, you have a mold in you! You may have Adenovi- ruses quietly slipping into your blood stream and tissues from a tapeworm stage or mite you inhaled, or E. The significance of the mold is that it lowers your immunity, specifically and generally. So with mold toxins present, Adenovirus, fleeing the dead tapeworm stage, mite, or E. But as soon as any cross the colon wall to invade your body, your white blood cells pounce on them. One place you do feel an attack is in your respiratory tract: lungs, bronchi, sinuses, nose, Eustachian tubes, inner ear, eyes or head. We do not taste it because manufacturers have been using more and more flavorings in food. Vinegar is used instead of calcium propionate in some breads but, again, the plastic ruins its effectiveness. None of the old fashioned tortillas (made with just corn, water, lime) that I tested had any mold, even without propionate added! The two likely sources for the mold spores are: in the flour to begin with, or just flying about the bakery and landing on the newly baked loaves. Bread flour in the grocery store is quite free of mold spores, so maybe it is the bakery that needs to change. Perhaps it is not possible to bake 24 hours a day in the same building, year after year, without bits of flour and moisture accumulating in the millions of tiny cracks and crevices that all buildings have and germinating mold. As soon as you feel a cold coming, ask yourself: what did you eat recently that might have been moldy? Cold cereal, hot cereal, bread, crackers, cookies, rice, other grains, fresh fruit, store bought fruit juice, nuts, syrups, pasta, honey? This lowers your immunity, allowing any Adenovirus to invade your weakest tissues. It will still take five or six hours for your white blood cells to re- cover their ability to capture viruses, for the “gag” to wear off. Wait twenty minutes to let viruses and bacteria in the dead larger parasites emerge. Zapping kills the escap- ees, though, to give a bit of relief, and the Bowel Program stops the invasive E. Do additional zapping as time permits until the Bowel Program has stemmed the invasion. If you eat cheese it will add Salmonella to your illness and you may develop a fever. Test yourself for the presence of molds to see if you are ac- complishing your goal. But if you stop immediately and eat only perfectly safe food, your illness will be over in the shortest time. Before starting to cook sterilize your kitchen sponge (microwave it for three minutes), and wash hands. The egg carton and egg exterior have Salmonella on them, so remove the eggs, replace the carton, wash the exterior of the eggs and then your hands again before cracking them. If you get a hefty dose of mold at the outset of your cold, the toxicity lasts quite a long time. In animal experiments reported by scientists, toxicity from mold usually lasted three weeks. When you decide to take some risks, make sure vitamin C has been added to the new food and mixed with it thoroughly. Our parents were supposed to teach us in childhood to distinguish between good and bad food. We rely on government agency assurances, like beef grades, expiration dates, approved food colors and additives. We land in a debacle such as the present one, where large segments of society are ill with uncontrollable behavior (called crime), suffer from hormone imbalances and sexual dis- turbances, are sidelined by chronic fatigue and new illness. If you are tracking Adenovirus using the electronic techniques in this book, you will see that it infects you immediately after eating coughed-on food. Then it disappears, evidently eaten up by your white blood cells, pro- vided there is no mold toxin in you. But if you do have a mold toxin in you, the virus spreads, multiplies and gives you a cold! There are three or four favorite homeopathic remedies for colds and eight or nine less common ones. To use them you read the symptoms listed and take the remedy with the closest match. Homeopathic Remedy For These Symptoms Aconitum early cold with fever, headache, hoarse cough Allium clear runny nose with burning of lips or eyes Arsenicum sneezing cold, frontal headache, tickling cough Belladonna high fever cold with flushed face, throbbing head Kali bi thick post nasal drip, colored discharge, sinus headache Spongia croupy cough Fig. There are lots more remedies with fascinating symptoms to try to match with your own. Books suggest that you start with a 6X or a 12X remedy, but success is more certain with 30X. They go right to the gateways of your cells and evict the tiny parasite, bacteria or virus stuck to the latch and trying to get in. Different homeopathic remedies go to different tissues, so you can only clear one tissue at a time. If you plan on trying this for yourself, order the set of cold remedies listed above (see Sources). If you plan on trying these start with a set of thyme , fenugreek, sage (for throat). Since both herbs and homeopathic remedies work on the principle of ejection, they could eject each other. Ultimately, the length of time your own white blood cells are bound and gagged decides how soon you are really cured of your cold. If you find a recipe that works for everybody in less than five hours, be sure to let everybody know. True Origins Of Viruses Your body can eliminate any virus in a short time, such as hours or days. At that time, we can theorize that a new large parasite was making its appearance.
Cardiac examination is significant for a normoactive precordium cheap clozapine 50 mg with amex depression zaps your energy, without a right ventricular heave or thrill cheap clozapine 100mg free shipping bipolar depression in adolescents. An ejection click at the upper left sternal border can often be detected purchase 50 mg clozapine with amex depression symptoms blaming others, and corresponds to the opening of the doming pulmonary valve clozapine 25mg fast delivery mood disorder nos dsm v. The murmur is of an ejection quality and of medium intensity, usually grade 3 or less, and is best appreciated at the left upper sternal border, with radiation to the back (Fig. S1 first heart sound, S2 second heart sound, A aortic valve closure, P pulmonary valve closure. Obstruction to blood flow across the pulmonary valve results in the elevation of right ventricular pressure over pulmonary arterial pressure. This pressure gradient causes blood flow across the pulmonary valve to be turbulent and consequently noisy (murmur). The murmur starts with a systolic click as a result of opening of thickened valve cusps and followed by systolic ejection murmur as blood crosses the stenotic valve. The murmur’s harshness increases with severity of stenosis, although in extreme cases due to resulting heart failure, the murmur may become softer. A systolic ejection murmur not preceded by a systolic click may suggest diagnosis other than pulmonary valve stenosis. Stenosis of the right ventricular outflow tract, below or above the valve with a normal valve present with a murmur similar to pulmonary stenosis, however, without the click. Pulmonary stenosis murmur is best heard over the left upper sternal border 10 Pulmonary Stenosis 137 either slightly diminished, secondary to decreased pulmonary artery pressure, or slightly increased, secondary to poststenotic pulmonary artery dilation. Moderate valvular stenosis is often well toler- ated in children, but produces clinical symptoms with advancing age. Severe valvular stenosis can lead to exercise-related chest pain, syncope, or sudden death. Cardiac examination is often significant for increased precordial activity, with a right ventricular heave and a palpable thrill in the area of the pulmonary valve at the left upper sternal border. The earlier the ejection click is detected at the upper left sternal border, the more severe is the stenosis. The murmur is of an ejection quality and of high intensity, usually grade 4 or more, and is best appreciated at the left upper sternal border, with radiation to the back. The P2 intensity is often diminished, secondary to decreased pulmonary artery pressure. Since the pulmonary valve in most cases does not open, an ejection click and P2 will not be present. As very little or no flow across the pulmonary valve occurs, the murmur will be quite soft. Murmurs of branch pulmonary stenoses are appreciated in the back, with radiation to the axillae. A continuous murmur in the back and axillae suggests significant bilateral branch pulmonary artery stenosis. Chest Radiography The heart size is often normal, except in critical pulmonary stenosis, when the heart size may be increased secondary to right atrial enlargement. A prominent main pulmonary artery notch from poststenotic dilation of the pulmonary artery can often be appreciated in older infants and children. Lung fields appear variably void of pulmonary vascular markings (black or anemic), reflecting reduced pulmonary blood flow from increasing stenosis. Chest radiography in children with branch and peripheral pulmonary artery stenoses is commonly normal, but there may be a difference in vascularity between the two lung fields. Right ventricular and right atrial enlargement occurs when stenosis is severe and complicated by right ventricular failure. Echocardiography Two-dimensional echocardiography demonstrates the abnormal pulmonary valve with restricted motion, and poststenotic dilation of the pulmonary artery. Measurements can be made of the pulmonary valve annulus and the branch pulmonary arteries and compared with normative data. Color Doppler demonstrates turbulent flow through the valve, and spectral Doppler produces a pulse wave from which the pressure gradient across the valve is estimated: • Mild stenosis – Doppler pressure gradient of 35 mmHg or less, or estimated right ventricular pressure less than half the left ventricular pressure. Two-dimensional echocardiography also demonstrates areas of supravalvular and branch pulmonary artery stenosis. Color and spectral Doppler can be similarly used to evaluate the flow and pressure gradients across the areas of obstruction. The entire right ventricular outflow must be sequentially examined, as multiple levels of obstruction may occur and impact the estimated pressure gradient across the pulmonary valve. Right ventricular development, hypertrophy, and systolic and diastolic function can be assessed. Right atrial size, presence of an interatrial communication, and direction of atrial septal flow can be demonstrated. In neonates with concern for critical pulmonary stenosis, patency of the ductus arteriosus can be determined. Cardiac Catheterization Cardiac catheterization is reserved for therapeutic intervention. For valvular pulmonary stenosis, hemodynamic data are recorded, and angiography is performed for func- tional assessment and annular measurement of the pulmonary valve. Balloon valvuloplasty successfully provides valve patency, and has supplanted surgical valvotomy as the choice treatment for this lesion. Varying degrees of pulmonary insufficiency result from this intervention, which is typically well tolerated by the hypertrophied right ventricle. Cardiac catheterization for supravalvular, branch, and peripheral pulmonary stenosis deserves special mention. Diagnostic cardiac catheterization is performed to provide a hemodynamic understanding of often multiple levels of obstruction, and also to provide angiographic pictures of the peripheral pulmonary vasculature. Because these lesions are characterized by ultrastructural changes such as fibrous intimal proliferation, they can be resistant to standard balloon angioplasty, and require the use of specialized equipment such as cutting balloons and stents, which provide variable results. Following successful balloon angioplasty of severely stenotic peripheral pulmo- nary arteries, reperfusion injury to the distal lung segment sometimes occurs, and is clinically characterized by cough, low-grade fever, hypoxemia, and corresponding segmental air space disease on chest radiograph. Other Diagnostic Modalities Magnetic resonance imaging can be useful in defining peripheral pulmonary vas- cular anatomy and pathology, while radionuclide lung perfusion scans can be useful for quantifying blood flow to each lung. Treatment Mild pulmonary stenosis produces no symptoms and no difference in life expectancy. Symptoms should not be attributed to mild pulmonary stenosis if stenosis is indeed mild. Moderate pulmonary stenosis is often treated with medical observation, and is typically well tolerated by infants and young children. Indications for catheter intervention include symptoms of fatigue and exercise intolerance, symptoms which often are experienced with increased age, even with stable stenosis. Severe pulmonary stenosis can be successfully treated by catheter-based balloon angioplasty. Surgical valvotomy is reserved for patients in whom balloon valvulo- plasty has been unsuccessful or for patients in whom multiple levels of obstruction are demonstrated. Critical pulmonary stenosis requires prompt initiation of prostaglandin infusion to maintain ductal patency and provide pulmonary blood flow. Following complete echocardiographic assessment, most neonates proceed to the cardiac catheterization laboratory for balloon valvuloplasty, after which the prostaglandin infusion is dis- continued. Occasionally, infundibular stenosis becomes apparent following balloon valvuloplasty, and a surgical Gore-tex shunt is required to maintain pulmonary blood flow. Though pulmonary valve patency has been established, many neonates continue to demonstrate moderate cyanosis, with SpO2 of 70–80%, which improves slowly over several months as the right ventricular compliance improves and decreases the degree of right to left atrial level shunt. An infant with a history of critical or severe pulmonary stenosis and pulmonary valvuloplasty requires pulse oximetry assessment at each visit.