Magnetic resonance imaging findings in giant cell arteritis.

PurposeGiant cell arteritis (GCA) is a systemic vasculitis that affects medium-to-large-caliber arteries. Early diagnosis and treatment is essential as involvement of the ophthalmic artery or its branches may cause blindness. Radiographic findings may be variable and non-specific leading to delay in diagnosis. We conducted a review of the literature on neuroimaging findings in GCA and present a retrospective case series from tertiary-care ophthalmic referral centers of three patients with significant neuroimaging findings in biopsy-proven GCA.MethodsRetrospective case series of biopsy-proven GCA cases with neuroimaging findings at the Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital between 2010-2015 were included in this study. Literature search was conducted using Google Scholar and Medline search engines between the years 1970 and 2015.ResultsWe report findings of optic nerve enhancement, optic nerve sheath enhancement, and the first description in the English-language ophthalmic literature, to our knowledge, of chiasmal enhancement in biopsy-proven GCA. We describe four main categories of neuroimaging findings that may be seen in GCA from our series and from past cases in the literature.DiscussionIt is essential that clinicians be aware of the possible radiographic findings in GCA. Appropriate and prompt treatment should not be delayed based upon these findings.

Enhanced measles surveillance during an interepidemic period in Victoria.

OBJECTIVE: To describe results of the first two years of enhanced measles surveillance in Victoria. DESIGN: Case series identified through enhanced measles surveillance. PARTICIPANTS AND SETTING: All measles cases notified to the Disease Control Section, Department of Human Services, Victoria, in 1997 and 1998. MAIN OUTCOME MEASURES: Proportion of notified cases laboratory confirmed as measles, rubella, or human parvovirus infection; identification of clusters (two or more linked cases of measles); and utility of the National Health and Medical Research Council clinical case definition for suspected measles. RESULTS: Rates of laboratory testing of notified cases improved after introduction of a paediatric phlebotomy service in July 1997, from 21 of 90 notified patients (23%) in the preceding six months, to 258 of 317 notified patients (81%) between July 1997 and December 1998. Of the 317, only 19 (6%) were laboratory confirmed with measles, while a further 26 (8%) were laboratory confirmed with human parvovirus infection (18) or rubella (8). Three clusters of measles, involving 11 cases, were identified during 1998. Use of the NHMRC case definition did not greatly improve the positive predictive value for diagnosis of measles above that of notification alone (14% versus 8%). CONCLUSIONS: Circulation of measles virus in Victoria in 1997 and 1998 appeared minimal. In this interepidemic period most notified cases of measles were not measles; to identify true cases, surveillance during an interepidemic period must include laboratory testing of notified cases.

Measles outbreak in young adults in Victoria, 1999.

OBJECTIVES: To describe an outbreak of measles in Victoria. DESIGN: Case series with cases identified through enhanced passive surveillance and outbreak-related active surveillance. SETTING: State of Victoria, 1999. MAIN OUTCOME MEASURES: Number of cases; epidemiological links and patterns of transmission; patient demographic features and vaccination status; complications. RESULTS: 75 cases were identified (74 laboratory-confirmed; and one epidemiologically linked to a laboratory-confirmed case), with onset between 11 February and 2 May 1999. The first case was in a 21-year-old woman who had recently holidayed in Bali and worked at a large cinema complex in Melbourne. Sixteen cases occurred in people who had contact with the index case at the cinema on one evening. The outbreak spread to regional Victoria and South Australia. Median age of patients was 22 years; 64 (85%) were born between 1968 and 1981, with only one patient in the age group targeted by the primary school component of the 1998 Australian Measles Control Campaign; this child had not been vaccinated. More than a third of patients (28) were hospitalised (total, 97 inpatient days), and five were healthcare workers. CONCLUSIONS: This outbreak was caused by international importation of measles virus. It highlights the change in epidemiology of measles in Australia, from a disease of childhood to one predominantly affecting young adults. A strong two-dose childhood vaccination program, vigilant surveillance, and rapid response to outbreaks will continue to be the basis of measles control, but better protection for young adults should be considered.

Fatal iatrogenic iodine toxicity in a nine-week old infant.

BACKGROUND: Povidone-iodine has been used since the 1950s for various labelled uses as a topical antiseptic. The toxicity of an excessive dose in internal use is described in this case report. CASE REPORT: A 9-week old infant was treated for colic by a pediatric gastroenterologist with loperamide and the elimination of nonhuman milk. Without improvement he was hospitalized and given an enema of 50 mL of povidone-iodine diluted in 250 mL of a bowel irrigant. The enema was promptly expelled and 50 mL of the described solution was given hourly for three doses by nasogastric tube. The infant was found lifeless three hours after the last dose and resuscitation was unsuccessful. Autopsy showed a corroded and necrotic intestinal tract, serous fluid in body cavities, a blood total iodine of 14,600 micrograms/dL, protein-bound iodine of 3,400 micrograms/dL and inorganic iodine of 11,700 micrograms/dL.

Disposition of nicotine and eight metabolites in smokers and nonsmokers: identification in smokers of two metabolites that are longer lived than cotinine.

The disposition of a single intravenous dose of 14C-nicotine was investigated in six cigarette smokers and six nonsmokers. Plasma and urinary elimination of both nicotine and cotinine was faster in smokers than in nonsmokers. In the urine of both smokers and nonsmokers, we identified nicotine and eight metabolites, including two new metabolites: metabolite A (3-hydroxycotinine glucuronide) and metabolite G (demethylcotinine delta 2',3'-enamine). Metabolites A and G were of particular interest because, in smokers, they both persisted longer than cotinine. This property renders them more sensitive than cotinine as potential indicators of passive exposure to cigarette smoke.

Mechanism of cold diuresis in the rat.

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

Effects of steady-state plasma vasopressin levels on the distribution of intrarenal blood flow on electrolyte excretion.

1. In order to evaluate the effects of arginine vasopressin (AVP) on the distribution of intrarenal blood flow and on electrolyte excretion, steady-state plasma AVP levels (4-8, 19-1, 44-3, and 100-6 micro u./ml.) were produced in anaesthetized dogs, which were hydrated to minimize endogenous anti-diuretic hormone (ADH) release. 2. The urinary excretion of sodium and potassium increased without change in their filtered loads during AVP infusion. 3. Measurement by the 133xenon washout method revealed diphasic blood flow shifts, as a function of the plasma AVP level, between compartment 1 (outer cortex) and compartment 2 (inner cortex and outer medulla) without change in compartment 3 (inner medulla). 4. In a separate study, the radioactive microsphere (15 micronm) method was used with a plasma AVP levels of 19-8 micronu./ml. Blood flow (expressed as % flow/g tissue) decreased in the outer cortex and increased in the inner cortex. 5. Total renal blood flow did not change during infusion of AVP. However, the values measured by 133xenon were lower than those measured by the microsphere method. 6. There was agreement between these two independent methods that blood flow shifted from outer to inner cortex, with no change in total renal flow, at similar plasma AVP levels (19-1 and 19-8 micronu./ml.). The relationship of these intrarenal circulatory changes to the increased electrolyte excretion is discussed.