Friday, November 28, 2014

Some important data about AAA...

OK... we are going to talk AAA, and this is not the American Alcoholic Anonymous! Abdominal Aortic Aneurysms kill, and kill fast when not diagnosed promptly. Here are some useful tips about this deadly condition so it will easy for you to recognized it.

Nonmodifiable risk factors for abdominal aortic aneurysm include older age, male sex, and a family history of the disorder. Starting at 50 years of age for men and 60 to 70 years of age for women, the incidence of aneurysms increases significantly with each decade. The risk of abdominal aortic aneurysm is approximately four times as high among men as among women and four times as high among people with a family history of the disorder as among those without a family history. Smoking is the strongest modifiable risk factor. Other, less prominent risk factors for abdominal aortic aneurysm include hypertension, an elevated cholesterol level, obesity, and preexisting atherosclerotic occlusive disease.

What are the recommendations for screening for abdominal aortic aneurysms?
Ultrasonography is the primary method used for screening and is highly sensitive (95%) and specific (100%). CT scanning and magnetic resonance imaging (MRI) are expensive, incur risks (radiation exposure from CT and risks associated with intravenous contrast material), and should not be used for screening but rather reserved for preinterventional planning. The current recommendations of the U. S. Preventive Services Task Force are a one-time screening in men 65 to 75 years of age who have ever smoked (grade B recommendation) and selective screening in men 65 to 75 years of age who have never smoked (grade C recommendation). Medicare also covers screening for patients with a family history of abdominal aortic aneurysm. Data from nonrandomized studies suggest that there may be subgroups of women who benefit from screening; however, this finding has not been prospectively validated.

What are the indications for surgical repair of an abdominal aortic aneurysm?
Under most circumstances, aneurysms should not be prophylactically repaired unless they are at least 5.5 cm in diameter. Nevertheless, there are occasions when repair of small aneurysms should be considered. Symptomatic aneurysms should be immediately repaired. Pain in the abdomen, back, or flank is the most common symptom, but aneurysms can produce many other symptoms or signs (e.g., hematuria or gastrointestinal hemorrhage). The rate of growth is another important predictor of rupture; aneurysms that expand by more than 0.5 cm in diameter over a period of 6 months should be considered for repair regardless of the absolute size. The observations that aneurysms rupture at a smaller size in women than in men and that women have higher rupture-related mortality than men have led some experts to recommend a diameter of 5.0 cm as the threshold for elective intervention in women. Other factors that are associated with an increased risk of rupture and may prompt repair at a threshold of less than 5.5 cm include the presence of a saccular aneurysm (most aneurysms are fusiform) and a family history of abdominal aortic aneurysm.

What surgical techniques are available for repair of an abdominal aortic aneurysm?

Two approaches to repairing aneurysms are currently available: open repair (performed since the 1950s) and endovascular repair (first performed in 1987). Endovascular repair, a less invasive approach, involves the intraluminal introduction of a covered stent through the femoral and iliac arteries; the stent functions as a sleeve that passes through the aneurysm sac, anchoring in the normal aorta above the aneurysm and in the iliac arteries below the aneurysm. To be eligible for endovascular repair, a patient must have appropriate anatomy, including iliac vessels that are of sufficient size to allow introduction of the graft and an aortic neck above the aneurysm that allows the proximal graft to be anchored without covering the renal arteries. Thus, with existing techniques, there are some infrarenal aneurysms that are not amenable to endovascular repair. The use of endovascular repair has grown steadily in the United States, and this procedure is currently performed in more than 75% of patients undergoing surgical intervention for abdominal aortic aneurysm, with a portion of the remaining patients having unsuitable anatomy. Endovascular repair confers an initial survival benefit; however, this benefit disappears over a period of 1 to 3 years. Endovascular repair and open repair are associated with similar mortality over the long term (8 to 10 years).

Thursday, November 6, 2014

Malaria - Quick review

Although Ebola has been all the furor in the recent weeks, fever in travelers is NOT Ebola most of the times. Depending on the region and season, the usual culprits are more likely than Ebola, these include malaria, dengue, yellow fever, chikungunia virus, hepatitis, salmonella and other intestinal bugs, multiple parasites among others. Here is the Q&A for malaria and babesia from this month's NEJM.

What is the annual incidence of malaria in the United States?
In the United States, the annual incidence of malaria is approximately 1500 cases. In 2010, a total of 1691 cases were reported to the Centers for Disease Control and Prevention (CDC), the largest number reported since 1980; P. falciparum, P. vivax, P. malariae, and P. ovale were identified in 58%, 19%, 2%, and 2% of cases, respectively.

How do malaria and babesiosis differ in appearance on a peripheral blood smear?
Intraerythrocytic parasites are seen in both malaria and babesiosis. Plasmodia metabolize heme to form an intracellular crystallized pigment, hemozoin. Although hemozoin is not invariably identified in cases of malaria, its presence reliably distinguishes malaria infection from babesia infection. Malaria parasites can be distinguished from B. [Babesia] microti by the presence of recognizable gametocytes (characteristically banana-shaped in Plasmodium falciparum and round, with a granular appearance, in nonfalciparum species). In addition, intracellular vacuoles and extracellular merozoites are unusual in malaria but common in babesiosis, and the classic “Maltese cross” (a tetrad of parasites budding at right angles) is unique to babesia species.

Which malaria species can remain dormant in the liver?
In the case of P. vivax and P. ovale, some sporozoites (immature malaria parasites) do not replicate immediately when they invade hepatocytes but remain dormant (as hypnozoites) for prolonged periods. The average time to relapse is approximately 9 months, but it can range from weeks to years. The interval to relapse depends on the strain (earlier with tropical strains and later with temperate strains), the initial inoculum, and host factors (e.g., febrile illnesses can trigger relapse associated with P. vivax). None of the commonly used prophylactic agents (chloroquine, mefloquine, doxycycline, or atovaquone–proguanil) eliminate hypnozoites. Primaquine, the only effective drug against dormant hypnozoites, has not been approved by the Food and Drug Administration for primary prophylaxis, but the CDC endorses its use for prophylaxis in Latin American countries where P. vivax predominates, because the drug can prevent both primary attacks and relapses caused by all species that are a source of malarial infection.

How is acute or recurrent P. vivax infection treated?
In patients with acute or recurrent malaria infection, treatment depends on the species and the resistance status in the area where the infection was acquired. P. falciparum is resistant to chloroquine in most regions in which it is endemic and resistant to mefloquine in parts of Southeast Asia. In contrast, nonfalciparum malaria parasites do not have substantial resistance to mefloquine, and the distribution of chloroquine-resistant P. vivax malaria is limited, occurring primarily in Indonesia and Papua New Guinea. After treatment is initiated, peripheral-blood smears should be obtained daily for 4 days (parasitemia is typically eliminated by day 4), on days 7 and 28 to confirm eradication, and at any time symptoms recur, suggesting treatment failure. In areas other than those with known chloroquine resistance, chloroquine, followed by a 14-day course of primaquine to prevent subsequent relapses, remains the standard treatment for P. vivax parasitemia. Given the risk of hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who receive treatment with primaquine, potential recipients should be tested for G6PD deficiency. Among patients with a contraindication to primaquine therapy, treatment with chloroquine alone carries a 20% risk of relapse; extended chloroquine prophylaxis can be offered to patients who have frequent relapses.