Pulse pressure is the difference between systolic and diastolic blood pressure, or the change in blood pressure seen

during a contraction of the heart.

Introduction Pulse pressure is the change in blood pressure seen during a contraction of the heart; formally, it's the systolic pressure minus the diastolic pressure, measured in mmHg. Usually, the resting pulse pressure in healthy adults is about 40 mmHg. Various studies have shown that a high pulse pressure is linked to an increased risk of heart attack, stroke, and heart failure. These studies have mostly been confined to populations from a single country, and it's not necessarily clear if the results can be generalized to all people worldwide. New results from the so-called Seven Countries Study, which have been published in the Archives of Internal Medicine, help answer this point.
http://www.healthandage.com/The-Importance-of-Pulse-Pressure

Dengue shock syndrome

From Wikipedia, the free encyclopedia
Jump to: navigation, search Dengue shock syndrome (DSS), also mistakenly referred to as dengue hemorrhagic fever (DHF), is characterized by dengue fever's symptoms of abdominal pain, hemorrhage, with the addition of circulatory collapse. Dengue hemorrhagic fever starts unexpectedly with extreme fevers, headache, sore throat, cough, nausea and vomiting. Dengue shock syndrome is the most severe case of dengue fever. The shock occurs after two to six days of symptoms, followed by collapse, weak pulse, and blueness around the mouth. Symptoms also include: easy bruising, blood spots, bleeding gums and nosebleeds. Dengue shock syndrome can be fatal. The mortality rate ranges from 6 to 30 percent, most commonly in children.

Contents
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1 Signs and Symptoms 2 Diagnosis 3 Risk Factors o 3.1 Case Studies 4 Treatment o 4.1 Case Studies 5 See also 6 References

[edit] Signs and Symptoms

The initial stages of an uncomplicated dengue infection consist of fever (up to 105 degrees Fahrenheit) and severe headache, which can also be accompanied by other symptoms such as chilliness, nausea and vomiting, rash, backache, and severe muscle ache.[1] As the infection progresses into dengue hemorrhagic fever (DHF), the blood and lymph vessels are damaged and bleeding (hemorrhage) from the nose, gums, or under the skin creates purplish bruises.[2] Dengue shock syndrome (DSS), the most severe form of dengue fever, includes all DHF symptoms, as well as its own symptoms. Initial signs of DSS include restlessness, cold clammy skin, rapid weak pulse, and narrowing of pulse pressure and/or hypotension.[3] The more dangerous symptoms include abdominal pain, massive hemorrhage, and circulatory collapse. The most threatening symptom of DSS is circulatory collapse, also known as shock, and it occurs due to the massive loss of fluid between the third and fifth days of illness.[4]

[edit] Diagnosis
Primarily, dengue virus is diagnosed clinically using blood tests. Two tests are performed two to three weeks apart.[2] A patient is tested positive for dengue when antibodies of the virus are detected in the blood. Polymerase Chain Reaction (PCR) can be used to confirm the diagnosis. There are four serotypes of the dengue virus that can be diagnosed in patients. These serotypes are not cross protective, which means the host can become infected repeatedly if the serotype is different with each infection.[5] Dengue shock syndrome has been hypothesized to be the result of one dengue serotype following infection by another serotype.[5] However, DSS can also develop without sequential infections. The primary concern of sequential infection is that it may increase risk of getting the syndrome. In order to determine whether or not a dengue infection is in the form of dengue shock syndrome, the patient must show symptoms of dengue hemorrhagic fever, as well as these symptoms: Weak rapid pulse Narrow pulse pressure (less than 20 mm Hg) Cold, clammy skin and restlessness

[edit] Risk Factors

There are multiple risk factors to acquiring dengue shock syndrome. Mosquitoes are the main transmitters of DSS. Once the aedes albopictus or aedes aegypti feeds on an infected individual the mosquito carries the disease for its entire life. The infected mosquito then feeds on another individual causing them to be infected. However, the most repeatedly seen causes of dengue shock syndrome are the four different dengue virus serotypes (set of antigens with the same characteristics). Each of these serotypes has the ability to initiate dengue shock syndrome. Another general risk factor is geography. Southeast Asia, Africa and the most southern parts of the United States are the most prevalent places to acquire the dengue viruses leading to DSS.

Furthermore, dengue shock syndrome has been frequently noticed in children under the age of 10. Dengue can be obtained through the genetic predisposition of the person or passed from mother to baby. The dengue virus serotypes are named dengue type 1,2,3, and 4. The four serotypes are extraordinarily similar, but have different strains of dengue virus. If an individual is infected with one serotype, then s/he has immunity to that virus. However the immunity applies to only that virus not to the others. Exposure to one serotype, in fact causes the individual to be more susceptible to dengue shock syndrome. The immunity produces specific antibodies to prevent the virus from attaching to the macrophage cells, which is the target cell that dengue viruses infect. If an individual is infected with a second serotype of dengue virus the bodys immune system will trigger, thinking that it is the serotype of the first infection. The antibodies attach to the serotype, assuming they are doing their job, however the virus still exist and continues to infect the person. This condition is known as antibody dependent enhancement. The person persists to be infected resulting in dengue hemorrhagic fever and dengue shock syndrome. Geography is a major risk factor of dengue shock syndrome. Dengue shock syndrome is most commonly seen in tropical areas such as Southeast Asia, Africa and the most southern parts of the United States. DSS was first reported in Southeast Asia in the 1970s. By the 1980s and 1990s DSS spread to India, Sri Lanka, and China. DSS is now a leading cause of hospitalization and death among children in Asia. The mosquitoes that carry the dengue viruses are unable to live in cool temperatures. However, climate changes, such as global warming, are predictors of the spread of dengue. The mosquitoes can live wherever water collects, whether by human activity (water storage containers) or rainfall. Urban cities are the most impacted by dengue viruses. The insects thrive in tropical and subtropical regions with urban settings and deforestation. The dengue viruses that lead to dengue shock syndrome have been found in many international travelers. Travelers serve as an important double role as potential victims of the disease and as vehicles for further spread of dengue.[1] Dengue has become more and more expanded across the world. Once travelers are infected by mosquitoes, they bring the virus into their country where more mosquitoes can feed off of them and infect other individuals. (See Case Studies for more information) The genetic predisposition of the victim is another major risk factor to acquiring dengue shock syndrome. Race and blood type can be a predicting factor of dengue shock sydrome. (See Case Studies for more information) Dengue has also been seen through vertical transmission, or passed from mother to baby. There are particularly two cases portraying the idea of vertical transmission of dengue. (See Case Studies for description)

[edit] Case Studies

There have been reports of international travelers being infected with dengue virus and later progressing to dengue shock syndrome. There are three particular studies that have been done of non-tourists to help estimate the risk for North American travelers. Of 627 American residents in Bangkok, only six were infected with dengue viruses from 1962-1963. The other two studies were done from 1993 to 1994. In 1993 there were nearly 30,000 troops deployed in Somalia, 59 of which were confirmed with dengue shock syndrome. The study done in 1994 was of 20,000

troops in Haiti, 30 (0.1%) of which were confirmed with dengue shock syndrome.[1] These studies were not extremely helpful when estimating the risk for North Americans however, it was concluded that emigrants to the infected countries, are at significant risk of acquiring dengue infection. Research has been provided relating to the genetic predisposition of individuals that are more vulnerable to get DSS. The studies compare ethnic groups and blood types. Certain populations and ethnic groups show increased proclivity to develop DHF or DSS while others only develop DF. In 1981, there was a ratio done in Cuba comparing the DHF/DSS risk for whites, blacks, and mixed. The ratio was 5.5:1:1.8. Thus, whites are more susceptible to dengue shock syndrome. A 1996 study done in Haiti further supports the idea of host ethnicity as a risk factor for DSS. Eighty-five percent of sera from 6-13 year olds living in Port-au-Prince, have the dengue virus antibody, however there were no dengue cases reported in the city. Accordingly, 185 dengue virus isolates were found from primarily Caucasian United States military personnel who were stationed in Haiti and were presented with dengue fever. This indicates that Caucasian adults are more vulnerable to the dengue viruses than are Haitian children. Likewise, Africans contained the dengue serotypes without retrieving DHF/DSS, whereas in Asia, two studies report a significantly higher incidence of DHF among Chinese compared to Malaysian males: another indicator of ethnicity being a risk factor to DSS. Although, there is not great detail about findings relating to blood type being a factor of DSS, there is evidence that, Thai children with blood group AB were more likely to develop grade three DHF upon secondary infection compared to children with O, A, or, B blood[6]. This is the first study with a relation between blood type and dengue viruses. There are two certain cases with evidence of vertical transmission that took place in 1996 during the Malaysian dengue outbreak. The first woman was 25 years old and had no history of major illness. She was admitted to the hospital for proteinuric pregnancy-induced hypertension. Throughout the next week she developed symptoms of dengue. After giving birth to her son, the symptoms started worsening. She became anemic and was given a blood transfusion. By the end of the week she was diagnosed with dengue. The doctors found IgM antibody specific to dengue virus in her blood. The infant seemed fine at first. The only problem was that he was pale and grunting. After getting the routine dose of vitamin K, he needed to be incubated with ventilatory support because he was not getting enough oxygen and was soon in respiratory distress. The infant had a blood specimen taken for culture tests. By the end of the second day of life he had a noticeable red rash, fever and irritability. Another blood specimen was performed for culture tests. Just like the mother, the infant then received whole blood transfusions. The infant died on day six of life. After the death, dengue virus type 2 was found in his blood from the first blood specimen. However, IgM antibody specific to dengue virus was not detected from either blood specimen[7]. This concludes that the infant did acquire the dengue virus type 2, but could not create the antibodies to help treat it. Thus, dengue virus was forwarded from the mother; because he had not been bitten by a mosquito, vertical transmission is the only explanation. The second case was awfully similar to the first. The mother was a 31 year old Malay woman. She immediately had symptoms of dengue when admitted to the hospital. Two months earlier, her husband was admitted to a different hospital because of dengue fever. On day nine, the woman went into a spontaneous labor and delivered a female. The mother was discharged from the hospital on day 13. Dengue virus type 2 was found in the blood sample from day two. Then the antibodies were found in the second blood sample from day six. Given the outcome of the

first case, the infant was brought to the special care nursery immediately after birth for close observation[7]. On the fourth day, the infant had a fever. The IgM antibody specific to dengue was found in blood samples from days six and 11 of life, but not in either of the samples from the first day of birth. The infant was fine, and discharged home on day 11. The infant did not have the dengue virus, yet had the antibodies. Since the mother had retrieved both the virus and the antibodies, this indicates that the antibodies were passed from the mother to the infant.

[edit] Treatment
The treatment for Dengue Shock Syndrome is very similar to that of Dengue Fever. Rest and increase of fluids are the two main methods of treatment that are administered. Within the last ten to twenty years a series of tests has been conducted to see if steroids also can impact the recovery rate.

[edit] Case Studies

In one of the many studies conducted, a randomized double-blind trail (both parties do not know who is receiving what medicine) was conducted which compared four drugs (one was a placebo) and their outcomes on the infected individuals. It was performed on 50 children suffering from dengue shock syndrome. It concluded that a drug called Dextran 70 (a plasma expander) provided the best reaction.[8] Another similar test conducted by the same group of doctors was conducted in 2005. It studied 383 children who were suffering from varying degrees of dengue shock syndrome. They were randomly assigned to one of three drugs, (one of which, like before, was a placebo). A drug called Ringer's Lactate (a fluid resuscitator) worked best on the children with moderately severe dengue shock syndrome. Dextran 70 and the placebo worked best on children with severe shock.[9] Yet another test was conducted on 230 Vietnamese children suffering from dengue shock syndrome which also yielded no clear results. The doctors took four fluids: Dextran 70, Gelatin, Ringer's Lactate, and a normal saline, and distributed them randomly. All the children survived, but the group who received Ringer's Lactate took the longest to recover.[10] A different group of doctors tried to use hydrocortisone to affect the outcome of dengue shock syndrome. They administered it randomly to 97 patients and evaluated their results based on mortality rate, duration of shock, and amount of replacement fluids that were required. They compared the results to a group of 47 children who were treated with contemporary drugs and 50 children who were not treated. The results concluded that hydrocortisone is of no value in the treatment of dengue shock syndrome.[10]