Cardiovascular, Lymphatic and Systemic Diseases
Cardiovascular & Lymphatic » Septic shock » Rheumatic fever » Schistosomiasis » Elephantiasis/Filariasis Systemic » Anthrax » Plague » Lyme disease » Dengue fever » Malaria
SEPTIC SHOCK Sepsis or septic shock is a systemic inflammatory response secondary to a documented infection. Consequently, sepsis is a continuum of detrimental host responses to infection that ranges from sepsis to septic shock and Multiple Organ Dysfunction Syndrome(MODS). Shock refers to a state of inability to maintain adequate tissue perfusion and oxygenation, ultimately causing cellular, and then organ system dysfunction. Pathophysiology » Inflammatory mediators are the key players in the pathogenesis. » The gram-positive and gram-negative bacteria induce a variety of proinflammatory mediators, including cytokines. Such cytokines play a pivotal role in initiating sepsis and shock. The bacterial cell wall components are known to release the cytokines; these include lipopolysaccharide (gram-negative bacteria), peptidoglycan (gram-positive and gramnegative bacteria), and lipoteichoic acid (grampositive bacteria). » An imbalance of homeostatic mechanisms leads to disseminated intravascular coagulopathy (DIC) and microvascular thrombosis causing organ dysfunction and death. The predominant hemodynamic feature of septic shock is arterial vasodilation. Diminished peripheral arterial vascular tone may result in dependency of blood pressure on cardiac output, causing vasodilation to result in hypotension and shock if insufficiently compensated by a rise in cardiac output. Vasoactive mediators cause vasodilatation and increase the microvascular permeability at the site of infection. Nitric oxide plays a central role in the vasodilatation of septic shock. Impaired secretion of vasopressin also may occur, which may permit the persistence of vasodilatation. Etiology » Most patients who develop sepsis and septic shock have underlying circumstances that interfere with the local or systemic host defense mechanisms. The most common disease states predisposing to sepsis are malignancies, diabetes mellitus, chronic liver disease, chronic renal failure, and the use of immunosuppressive agents. In addition, sepsis also is a common complication after major surgery, trauma, and extensive burns. » Respiratory tract infection and urinary tract infection are the most frequent causes of sepsis, followed by abdominal and soft tissue infections. » The use of intravascular devices is a notorious cause of nosocomially-acquired sepsis. » Multiple sites of infection may occur in 6-15% of patients.
» Lower respiratory tract infections are the cause of septic shock in 25% of patients. The following are common pathogens: ♪ Streptococcus pneumoniae ♪ Klebsiella pneumoniae ♪ Staphylococcus aureus ♪ Escherichia coli ♪ Legionella species ♪ Haemophilus species ♪ Anaerobes ♪ Gram-negative bacteria ♪ Fungi » Urinary tract infections are the cause of septic shock in 25% of patients, and the following are the common pathogens: ♪ E. coli ♪ Proteus species ♪ Klebsiella species ♪ Pseudomonas species ♪ Enterobacter species ♪ Serratia » Soft tissue infections are the cause of septic shock in 15% of patients, and the following are the common pathogens: ♪ S. aureus ♪ Staphylococcus epidermidis ♪ Streptococci ♪ Clostridia » GI tract infections are the cause of septic shock in 15% all patients, and the following are the common pathogens: ♪ E. coli ♪ Streptococcus faecalis ♪ Bacteroides fragilis ♪ Acinetobacter species ♪ Pseudomonas species ♪ Enterobacter species ♪ Salmonella species Risk factors » Extremes of age ( <10 y and >70 y) » Primary diseases ♪ Liver cirrhosis ♪ Alcoholism ♪ Diabetes mellitus ♪ Cardiopulmonary diseases ♪ Solid malignancy ♪ Hematologic malignancy » Immunosuppression ♪ Neutropenia ♪ Immunosuppressive therapy ♪ Corticosteroid therapy ♪ Intravenous drug abuse ♪ Compliment deficiencies ♪ Asplenia » Major surgery, trauma, burns » Invasive procedures ♪ Catheters ♪ Intravascular devices ♪ Prosthetic devices ♪ Hemodialysis and peritoneal dialysis catheters ♪ Endotracheal tubes » Prior antibiotic treatment » Prolonged hospitalization » Other factors - Childbirth, abortion, and malnutrition Signs and Symptoms » Temperature greater than 38°C or less than 36°C. » Heart rate greater than 90. » Respiratory rate greater than 20 per minute. » WBC count more than 12,000/µL. » Chills are a secondary symptom associated with fever, which is a consequence of increased muscular activity that produces heat and raises the body temperature.
» Sweating occurs when the hypothalamus returns to its normal set point and senses the higher body temperature, stimulating perspiration to evaporate excess body heat. » Alteration in mental function often occurs: apprehension, anxiety, agitation, and, eventually, coma are manifestations of severe sepsis. » Hyperventilation with respiratory alkalosis is a common feature of patients with sepsis secondary to stimulation of the medullary respiratory center by endotoxins and other inflammatory mediators. Diagnosis » PE, v/s » Observe patients for systemic signs of inadequate tissue perfusion. In the early stages of sepsis, cardiac output is well maintained or even increased. The vasodilation may result in warm skin, warm extremities, and normal capillary refill (warm shock). As sepsis progresses, stroke volume and cardiac output fall, the aeg start to manifest signs of hypoperfusion(cool skin, cool extremities, and delayed capillary refill or cold shock). » CBC with dif count (Hgb, WBC, plt). » Assess renal and hepatic functions (serum creatinine, BUN, ALT, AST, albumin). Treatment » The principles in the management of septic shock, based on current literature, include the following components: ♪ Early recognition ♪ Early and adequate antibiotic therapy ♪ Source control ♪ Early hemodynamic resuscitation and continued support ♪ Corticosteroids (refractory vasopressordependent shock) ♪ Proper ventilator management with low tidal volume in patients with ARDS ♪ Vasopressor drugs: Dopamine, Epinephrine, Norepinephrine Nursing Interventions » Assist doctor in management » Medications as ordered » Administer oxygen as ordered » Assist in intubation » Aseptic technique
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pericardial involvement usually resolves without serious sequelae. However, rheumatic endocarditis results in permanent and often crippling adverse effects. Rheumatic endocarditis first manifests anatomically as tiny, translucent vegetations or growths along the margins of the valve leaflets. These become the starting point of a process that gradually thickens the leaflets, causing them to shorten and thicken, preventing them from closing completely. As a result, blood flows backward through the valve (valvular regurgitation). The most common site of valvular regurgitation is the mitral valve. In some patients, the margins of the valve leaflets become adherent or the chordate tendineae fuse resulting in valvular stenosis. Occurs most often in school-age children. ARF presents 2-6 wks following an untreated or partially treated GABHS infection of the URT Prompt tx of strep throat with antibiotics can prevent the development of ARF.
Epidemiology » As a sequel of beta-streptococcal exposure, ARF occurs during school years when streptococcal pharyngitis is most prevalent. Similarly, prevalence is higher in the colder months of the year when streptococcal pharyngitis is most likely to occur. Signs and Symptoms » Guidelines of diagnosis used by the American Heart Association include major and minor criteria (i.e., modified Jones criteria). In addition to evidence of a previous streptococcal infection, the diagnosis requires 2 major Jones criteria or 1 major plus 2 minor Jones criteria.
RHEUMATIC FEVER Rheumatic fever causes chronic progressive damage to the heart and its valves. The association between sore throat and rheumatic fever was not made until 1880. The dramatic decline in the incidence of rheumatic fever is thought to be largely owing to antibiotic treatment of streptococcal infection Pathophysiology » Acute Rheumatic Fever (ARF) is a sequel of a previous group A streptococcal infection, usually of the upper respiratory tract. » This condition is non-infectious in the sense that tissues are not invaded and directly damaged by the streptococci. Injury is caused by an inflammatory or sensitivity reaction to streptococci. Leukocytes accumulate in the affected tissues and form nodules, which eventually are replaced by scar tissue. The myocardium is involved in the inflammatory process. Rheumatic myocarditis develops which temporarily weakens the contractile power of the heart. The pericardium is affected, and rheumatic pericarditis occurs during the acute illness. Myocardial and
Major criteria » Carditis: This occurs in as many as 40% of patients and may include cardiomegaly, murmur, congestive heart failure, and pericarditis, with or without valvular disease. » Migratory polyarthritis: This condition occurs in 75% of cases and involves large joints; may last up to 4 wks. » Subcutaneous nodules (ie, Aschoff bodies): These nodules occur in 10% of patients and are edematous, fragmented collagen fibers. They are round, firm, painless, free-moving nodules on the extensor surfaces of the wrists, elbows, and knees; usually disappear after 1-2 wks » Erythema marginatum: This condition occurs in about 5% of cases; characterized by macular or popular, non-itchy rash on the trunk and proximal extremities. » Chorea (also known as Sydenham chorea and "St Vitus dance"): This characteristic movement disorder occurs in 5-10% of cases. Sydenham chorea consists of rapid, purposeless,
erratic, jerky, uncoordinated, involuntary movements of the face and upper extremities. Onset may be delayed for several months and may cease when the patient is asleep; usually resolves completely within 6 mos. Minor criteria » Clinical findings include arthralgia, fever and previous history of ARF » Laboratory findings include elevated acute phase reactants (e.g., erythrocyte sedimentation rate, C reactive protein), a prolonged PR interval, and supporting evidence of antecedent group A streptococcal infections (i.e., positive throat culture or rapid streptococcal screen and an elevated or rising streptococcal antibody titer). Other Assessment Finding » Elevated antistreptolysin O (ASO) titer » Weight loss, HA, malaise, diaphoresis and pallor Diagnosis » Jones criteria » Streptococcal antibody tests disclose preceding streptococcal infection. » Isolate group A streptococci via throat culture Complications » Rheumatic Heart Disease: affectation of cardiac valves, particularly the mitral valve, as evidenced by heart murmur » Mitral stenosis; pericarditis; cardiomegaly; CHF Treatment » Penicillin G benzathine IM » Prednisone (glucocorticoid) » Naproxen (NSAID) » Haloperidol may be helpful in controlling chorea Nursing Interventions » Antibiotics as ordered; completing the course of antibiotics minimizes the risk of developing ARF (and subsequently rheumatic heart disease) » Salicylates and anti-inflammatory agents » Emphasize importance of long-term cardiac reevaluation and regular prophylactic antibiotics » Maintain hydration » Control joint pain and inflammation with massage » Limit physical exercise in child with carditis » Monitor symptoms of complications (pulmonary HPN), CHF, thromboemboli, valvular disease, arrhythmias
individuals with new schistosomal infections. It may correspond to the first cycle of egg deposition and is associated with marked peripheral eosinophilia and circulating immune complexes. It is most common with S japonicum and S mansoni infections and is most likely to occur in heavily infected individuals after primary infection. Symptoms usually resolve over several weeks, but the syndrome can be fatal. Early treatment with cidal drugs may exacerbate this syndrome and necessitate concomitant glucocorticoid therapy. » Mild maculopapular skin lesions may develop in acute infection within hours after exposure to cercariae. Significant dermatitis is rare with the major human schistosomal pathogens, probably because the invading and developing cercariae are minimally immunogenic. However, abortive human infection with schistosomal species that rely on other primary hosts may cause marked dermatitis or swimmer's itch. This self-limited process may recur more intensely with subsequent exposures to the same species. Epidemiology » Highly endemic in Regions VIII, X, XI and XII Incubation Period » 2-6weeks Mode of Transmission » Skin penetration of infective cercariae through wading, swimming in infested waters » Not transmissible from person to person Signs and Symptoms » Swimmer’s itch: itchiness within 24hours; redness; and pustule formation at the point of entry of cercariae lasting 2-3days. » Diarrhea; abdominal pain. » Katayama fever: fever; generalized lymphadenopathy; hepatosplenomegaly 2-3weeks after initial infection and last for 1-2months. Diagnosis » S/E: ID of eggs » Liver & rectal biopsy Complications » Portal cirrhosis; cor pulmonale (hypertrophy of LV resulting from lung disease); myocardial damage. Treatment » Praziquantel PO Nursing Interventions » Proper disposal of excreta » Avoid wading in infested waters » Elimination of intermediate host » Maintain nutrition ELEPHANTIASIS Or Lymphatic Filariasis, is a rare disorder of the lymphatic system caused by parasitic worms such as Wuchereria bancrofti and Brugia malayi, all of which are transmitted by mosquitos(Aedes poicilus, Culex fatigans, Anopheles flavirostris). Inflammation of the lymphatic vessels causes extreme enlargement of the affected area, most
SCHISTOSOMIASIS Also Bilharziasis or snail fever is a human disease syndrome caused by infection from one of several species of parasitic trematodes of the genus Schistosoma. This is a major source of morbidity and mortality for developing countries in Africa, South America, the Caribbean, the Middle East, and Asia. Most human schistosomiasis is caused by Schistosoma haematobium, Schistosoma mansoni, or Schistosoma japonicum.
Pathophysiology » Acute schistosomiasis (i.e., Katayama fever) is a serum sickness–like illness that develops after several weeks in some, but not most,
commonly a limb or parts of the head and torso. It occurs most commonly in tropical regions. Pathophysiology » Larvae from the mosquito migrate to the lymphatics, where they develop into threadlike adult worms within 6 to 12 months. Gravid adult females produce microfilariae that circulate in blood. Epidemiology » Phil stat: 2.5/100,000 population » Distribution: Camarines Norte/Sur, Sorsogon, Quezon, Albay, Mindoro, Bohol, Samar, Palawan, Sulu, Tawi-Tawi, Basilan Mode of Transmission » Bite of mosquito Diagnosis » Fresh blood smear » Bentonite Flocculation Test Signs and Symptoms » Acute: fever, malaise, chills » Chronic: lymphadenitis, swelling of scrotum, lymphatic channel affected; eosinophilia
a protective antigen, a lethal factor, and an edema factor. The protective antigen is an 83-kd protein that binds to cell receptors within a target tissue. Once bound, a fragment is cleaved free to expose an additional binding site. This site can combine with edema factor to form edema toxin or with lethal factor to form lethal toxin. Edema toxin acts by converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cellular cAMP levels are increased, leading to cellular edema within the target tissue. Lethal factor is not well understood, but recent work suggests that it may inhibit neutrophil phagocytosis, lyse macrophages, and cause release of tumor necrosis factor and interleukin 1. Epidemiology » A zoonotic disease; spores can remain viable in soil for years. » Livestock can become infected and can transmit infection to humans on contact with infected animals or animal products (hides, hair, wool, meat). Incubation Period » 2-60 days Mode of Transmission » Ingestion, inhalation or ingestion Signs and Symptoms » Cutaneous: pruritic papule or vesicle which enlarges and ulcerates in 1-2days; a central black aschar forms (malignant pustule); lesion is painless but with surrounding edema » Inhalational: fever; chills; non-productive cough; chest pain; headache; myalgia; malaise; pleural effusion; septic shock » GI: N&V; anorexia; abdominal pain; ascites; hematemesis; bloody diarrhea Diagnosis » CXR » G/S and culture of blood, pleural fluid, CSF, skin discharges, tissue biopsy specimen Treatment » Penicillin » Ciprofloxacin Nursing Interventions/Considerations » Standard precaution » Meds as ordered » Post-exposure prophylaxis » Anthrax vaccine Prognosis » high mortality for inhalational and GI anthrax
Treatment » Diethylcarbamazine citrate (Beltrazan) » AH or corticosteroid » Surgical Nursing Interventions » Meds as ordered » Vector control » Health education in endemic areas ANTHRAX The term anthrax means coal in Greek, and the disease is named after the appearance of its cutaneous form. Anthrax is described in the Old Testament, by the poet Virgil, and by the Egyptians. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. Anthrax is caused by inhalation, skin exposure, or gastrointestinal (GI) absorption. Disease caused by inhalation is usually fatal, and symptoms usually begin days after exposure. This delay makes the initial exposure to Bacillus anthracis difficult to track Can be grown in laboratories and is a potential biowarfare agent.
Pathophysiology » Virulence depends on the bacterial capsule and the toxin complex. The capsule is a poly-D-glutamic acid that protects against leukocytic phagocytosis and lysis. Anthrax toxins are composed of 3 entities:
PLAGUE The plague has caused more fear and terror than perhaps any other infectious disease in the history of humankind. It has laid claim to nearly 200 million lives and has brought about monumental changes, such as the end of the Dark Ages and the advancement of clinical research in medicine. Alexandre Yersin isolated the plague bacillus, developed an antiserum to combat the disease, and postulated its connection with fleas and rats during the epidemic of 1894. The plague bacillus was named Yersinia pestis in his memory.
Although, the plague has been considered a disease of the Middle Ages, recent interest has been spurred by concerns over its use as a potential biological weapon. Aerosolized Y. pestis, causing primary pneumonic plague, has been recognized by bioterrorism experts as having one of the highest potentials for adverse public health impacts. In addition to the concern over its use in acts of terrorism, there are further reasons that may cause a dramatic increase in the number of plague cases worldwide in the years to come. One reason may be the climatic change brought about by global warming. This change is ideal for increasing the prevalence of Y. pestis in the host population. A recent study has estimated a more than 50% increase in the plague host prevalence with an increase of 1degree centigrade of the temperature in spring. Another reason may be the increasing population explosion worldwide, which is bringing humans into ever-increasing contact with wildlife. Lastly, the dramatic population increase will contribute to conditions of overcrowding and poor sanitation—conditions ripe for plague hosts and vectors to flourish in. Pathophysiology » Three forms of the plague exist: bubonic plague, pneumonic plague, and septicemic plague. The bubonic form of the plague involves the pathognomonic "bubo" and is caused by deposition of the bacillus in the skin by the bite of an infected vector. If the vector is a flea, bacillus proliferates in the flea's esophagus, preventing food entry into the stomach. To overcome starvation, the flea begins a blood-sucking rampage. Between its attempts to swallow, the distended bacillus-packed esophagus recoils, depositing the bacillus into the victim's skin. » The bacillus invades nearby lymphoid tissue, producing the famous bubo, an inflamed, necrotic, and hemorrhagic lymph node. Spread occurs along the lymphatic channels toward the thoracic duct, with eventual seeding of the vasculature. Bacteremia and septicemia ensue. The bacillus potentially seeds every organ, including the lungs, liver, spleen, kidneys, and rarely even the meninges. » The most virulent form, pneumonic plague, results from direct inhalation of the bacillus, which occurs from close contact of infected hosts or from aerosolized bacteria such as may occur if used as a biological weapon. A severe and rapidly progressive multilobar bronchopneumonia ensues with subsequent bacteremia and septicemia. Secondary pneumonic plague is caused when an infected patient seeds his or her lungs and airways. » The third type of plague is a primary septicemic plague. This is hypothesized to occur when the bacillus is deposited in the vasculature, bypassing the lymphatics. Early dissemination with sepsis occurs but without the formation of a bubo. This usually is observed in bites to the oral, tonsillar, and pharyngeal area and is believed to occur because of the vascularity of the tissue and short lymphatic distance to the thoracic duct. Epidemiology » From 1967-1993, the World Health Organization has reported an annual average of 1666 cases of the plague. Mode of Transmission » Bite of vector, rat flea Xenopsylla cheopis » Contact with infected tissue or body fluid » Inhalation
Signs and Symptoms » Fever ; chills; myalgias; sore throat; malaise » Enlarged, painful, swollen lymph node (bubo) » Abdominal pain » Nausea, vomiting (bloody at times) » Constipation, diarrhea, and black or tarry stools » Cough, which may be productive of bloody sputum » Shortness of breath » Stiff neck Diagnosis » CBC: elevated WBC » U/A: hematuria, proteinuria » ABG: hypoxia and/or acidosis » G/S, culture of blood, sputum or bubo aspirate Treatment » Gentamicin IV/IM » Supportive Nursing Considerations » Medications as ordered » Universal precaution (goggles, gloves, gown; mask if pneumonic) LYME DISEASE Is a multi-system infection commonly affecting the skin, CNS, heart and joints caused by the spirochete Borrelia burgdorferi. The bacterium is inoculated into the skin by a tick bite. The tick is almost always of the genus Ixodes. (ticks live in wooded areas and survive by attaching to a host) Pathophysiology » Once in the skin, the spirochete can (1) be overwhelmed and eliminated by host defense mechanisms; (2) remain viable and localized in the skin where it produces the pathognomonic skin lesion, or erythema migrans (EM); or (3) disseminate through the lymphatics or blood. Hematogenous dissemination can occur within days to weeks of initial infection; the organism can travel to the skin, heart, joints, CNS, and other parts of the body. Epidemiology » In 2001, the CDC reported 17,029 cases and, in 2002, that number rose to 23,763—a 40% increase. Year-to-year variation can be significant. More than 95% of cases come from 12 states (Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin). Even within these states, incidence can be quite variable from county to county and even neighborhood to neighborhood. Incubation Period » 14-23 days Mode of Transmission » Vector-borne
Signs and Symptoms » Bull’s eye rash or Erythema Migrans (a small red pimple develops at the site of bite that spreads into a ring-shaped rash) usually found in most parts of the body (1-33 days later; average, 7-10 days). The size varies enormously (as large as 70 cm; average, 16 cm) and depends on disease duration. EM usually is flat, round, or oval and monocyclic but nonpruritic » Flu-like symptoms (HA, stiff neck, myalgia, fatigue) » Arthralgia » Neurological and cardiac complications » Progression of arthritis Diagnosis » Aeg history » Dermatologic findings: Classic EM is an erythematous papule or macule that occurs at the site of the tick. » Elevated IgM Treatment » Amoxicillin » Doxycycline » Cefuroxime » Erythromycin Nursing Interventions » Ascertain if the aeg was exposed to deer ticks » Gently remove the tick with tweezers, wash the skin with antiseptic, and dispose of the tick by flushing it down the toilet; the tick may also be placed in a sealed jar for inspection by the health care provider. » Obtain a blood test 4-6 wks after a bite to detect the presence of the disease (testing before this time is not reliable) » Instruct the client to avoid wooded, grassy areas, esp in summer months » Instruct aeg to wear light colored, long-sleeved tops, long pants. Closed shoes and hats while outside » Instruct client to use tick repellent DENGUE Dengue has been called the most important mosquito-transmitted viral disease in terms of morbidity and mortality. Dengue fever is a benign acute febrile syndrome occurring in tropical regions. In a small proportion of cases, the virus causes increased vascular permeability that leads to a bleeding diathesis or disseminated intravascular coagulation (DIC) known as dengue hemorrhagic fever (DHF). In 20-30% of DHF cases, the patient develops shock, known as the dengue shock syndrome (DSS). Worldwide, children younger than 15 years comprise 90% of DHF subjects; however, in the Americas, DHF occurs in both adults and children Dengue is a homonym for the African ki denga pepo, which appeared in English literature during an 1827-28 Caribbean outbreak. The first definite clinical report of dengue is attributed to Benjamin Rush in 1789, but the viral etiology and its mode of transmission via mosquitoes were not established until the early 20th century. EA: DEN-1, DEN-2, DEN-3, DEN-4, Chikungunya virus Also called breakbone fever
Pathophysiology » Dengue viral infections frequently are not apparent. Classic dengue primarily occurs in nonimmune, nonindigenous adults and children. Symptoms begin after a 5 to 10 days incubation period. DHF/DSS usually occurs during a second dengue infection in persons with preexisting actively or passively (maternally) acquired immunity to a heterologous dengue virus serotype. Illness begins abruptly with a minor stage of 2-4 days duration followed by rapid deterioration. Increased vascular permeability, bleeding, and possible DIC may be mediated by circulating dengue antigen-antibody complexes, activation of complement, and release of vasoactive amines. In the process of immune elimination of infected cells, proteases and lymphokines may be released and activate complement coagulation cascades and vascular permeability factors. Epidemiology » Phil stat: 29.8/100,000 population » Source: infected persons » Common during rainy season » Infants and children mostly affected generally 0-9years old Incubation Period » 4-6days (min 3days, max 10days) Mode of Transmission » Day biting female mosquitoes (Aedes aegypti, Aedes albopictus) Signs and Symptoms » Grade I ♪ Fever; (+) tourniquet test; non-specific symptoms; abdominal sign; Herman’s sign (petechiae) » Grade II ♪ Grade I + bleeding (epistaxis, melena, gingival bleeding, coffee ground vomitus) » Grade III ♪ Grade II + circulatory collapse (hypotension, rapid & weak pulse, cold clammy skin » Grade IV ♪ Grade III + shock with undetectable BP & P Delayed capillary refill may be the first sign of intravascular volume depletion. Hypotension usually is a late sign in children. This child's capillary refill at 6 seconds was delayed well beyond a normal duration of 2 seconds. Diagnosis » Tourniquet test: assesses capillary fragility » CBC: leukopenia, thrombocytopenia, low hct » Dengue blot test
Treatment » Symptomatic and supportive » No specific antiviral treatment » Avoid aspirin Nursing Interventions » Monitor for signs of bleeding and fall in BP » Epistaxis: lean forward » Gingival bleeding: ice chips » Hematemesis: NPO Prognosis » Grade I & II: good » Grade III: guarded » Grade IV: serious, high mortality rate
Treatment » Chloroquine + Sulfadoxine/Pyrimethamine (CQ+SP) – 1st line drug in the treatment of probable malaria and confirmed Pf. » Artemether-Lumefantrine (Co-Artem TM) – 2nd line drug; given only to microscopically confirmed Pf which did not respond to CQ+SP. » Quinine + Tetracycline/Doxycycline – 3rd line drug; should be given to those who did not respond to CoArtem or if CQ+SP is not available. » N.B.: Tetracycline and Doxycycline are conrtaindicated for pregnant women and children under 8years old; instead give Quinine with Clindamycin.
MALARIA » Term malaria is derived from Latin words mal (bad) and aria (air). » Infection transmitted by female Anopheles mosquito, caused by Plasmodium falciparum(most fatal), P. vivax, P. ovale, P. malariae. » at high risk are pregnant women and children » Sexual cycle in mosquito; asexual cycle in human rbc » Pf: malignant tertian malaria » Pv: benign tertian malaria » Po: benign tertian malaria » Pm: quartan malaria Pathophysiology » The degree of damage to the tissue depends mainly on the parasitic concentration » Red cell changes: » Low deformability » High adhesion » High fragility » Low oxygen transport » Hemolysis leading to anemia » Rupture of infected and non-infected RBC (blackwater fever) » Organ damage: spleen, liver, brain, kidneys Epidemiology » Phil stat: 52/100,000 population Incubation Period » Pf: 10-13days » Pm: 27-37days or up to years » Po: 11-26days » Pv: 12-21days Mode of Transmission » Bite of female Anopheles Signs and Symptoms » Stages ♪ Cold: chilling: 10-15minutes (hot water bath on soles) ♪ Hot: 41degrees fever (TSB, antipyretics) ♪ Diaphoretic (increase fluids, rest) Diagnosis » Symptomatic » Malarial smear (peak of fever) » IFA