GANGLION CYSTS

GANGLION CYSTS

Ganglion cysts are noncancerous lumps that most commonly develop along the tendons or joints of your wrists or hands. They also may occur in the ankles and feet. Ganglion cysts are typically round or oval and are filled with a jellylike fluid.

Small ganglion cysts can be pea-sized, while larger ones can be around an inch (2.5 centimeters) in diameter. Ganglion cysts can be painful if they press on a nearby nerve. Their location can sometimes interfere with joint movement.

Symptoms

The lumps associated with ganglion cysts can be characterized by:

·         Location. Ganglion cysts most commonly develop along the tendons or joints of your wrists or hands. The next most common locations are the ankles and feet. These cysts can occur near other joints as well.

·         Shape and size. Ganglion cysts are round or oval and usually measure less than an inch (2.5 centimeters) in diameter. Some are so small that they can't be felt. The size of a cyst can fluctuate, often getting larger when you use that joint for repetitive motions.

·         Pain. Ganglion cysts usually are painless. But if a cyst presses on a nerve — even if the cyst is too small to form a noticeable lump — it can cause pain, tingling, numbness or muscle weakness.

Causes

No one knows exactly what causes a ganglion cyst to develop. It grows out of a joint or the lining of a tendon, looking like a tiny water balloon on a stalk, and seems to occur when the tissue that surrounds a joint or a tendon bulges out of place. Inside the cyst is a thick lubricating fluid similar to that found in joints or around tendons.

Risk factors

Factors that may increase your risk of ganglion cysts include:

·         Your sex and age. Ganglion cysts can develop in anyone, but they most commonly occur in women between the ages of 20 and 40.

·         Osteoarthritis. People who have wear-and-tear arthritis in the finger joints closest to their fingernails are at higher risk of developing ganglion cysts near those joints.

·         Joint or tendon injury. Joints or tendons that have been injured in the past are more likely to develop ganglion cysts.

Diagnosis

During the physical exam, your doctor may apply pressure to the cyst to test for tenderness or discomfort. He or she may try to shine a light through the cyst to determine if it's a solid mass or filled with fluid.

Your doctor might also recommend imaging tests — such as X-rays, ultrasound or magnetic resonance imaging (MRI) — to rule out other conditions, such as arthritis or a tumor. MRIs and ultrasounds also can locate hidden (occult) cysts.

A ganglion cyst diagnosis may be confirmed by aspiration, a process in which your doctor uses a needle and syringe to draw out (aspirate) the fluid in the cyst. Fluid from a ganglion cyst will be thick and clear or translucent.

Treatment

Ganglion cysts are often painless, requiring no treatment. Your doctor may suggest a watch-and-wait approach. If the cyst is causing pain or interfering with joint movement, your doctor may recommend:

·         Immobilization. Because activity can cause the ganglion cyst to get larger, it may help to temporarily immobilize the area with a brace or splint. As the cyst shrinks, it may release the pressure on your nerves, relieving pain. Avoid long-term use of a brace or splint, which can cause the nearby muscles to weaken.

·         Aspiration. In this procedure, your doctor uses a needle to drain the fluid from the cyst. The cyst may recur.

·         Surgery. This may be an option if other approaches haven't worked. During this procedure, the doctor removes the cyst and the stalk that attaches it to the joint or tendon. Rarely, the surgery can injure the surrounding nerves, blood vessels or tendons. And the cyst can recur, even after surgery.

LEPTOSPIROSIS

LEPTOSPIROSIS

BACKGROUND

• Leptospirosis is a disease that is caused by spirochete bacteria in the genus Leptospira. There are 10 pathogenic species, and more than 250 pathogenic serovars.
• While leptospirosis occurs worldwide, it is more common in tropical or sub-tropical climates.
• It is estimated that more than 1 million cases occur worldwide annually, including almost 60,000 deaths.
• In the United States, approximately 100–150 leptospirosis cases are reported annually. Puerto Rico reports the majority of leptospirosis cases, followed by Hawaii.
• Outbreaks of leptospirosis tend to occur after heavy rainfall or flooding in endemic areas, especially areas with poor housing and sanitation conditions.

TRANSMISSION

• Leptospires are spread by the urine of infected animals (rodents, dogs, livestock, pigs, horses, wildlife).
• The bacteria can survive for weeks to months in urine-contaminated water and soil.
• People can be infected through 
• Direct contact with the urine or reproductive fluids from infected animals
• Contact with urine-contaminated water (floodwater, rivers, streams, sewage) and wet soil
• Ingestion of food or water contaminated by urine or urine-contaminated water.
• Transmission occurs through mucous membranes, conjunctiva, and skin cuts or abrasions.

• Human-to-human transmission is very rare but has been documented through sexual intercourse and breastfeeding. Transmission has also rarely occurred through animal bites.
• High-risk activities can include wading, swimming, or boating in floodwater or freshwater (rivers, streams, lakes) that may be contaminated with animal urine. Some actions like prolonged immersion in, submerging head in, or swallowing contaminated water can particularly increase risk.
• Other high risk activities can include direct contact with animals and activities that can lead to skin abrasions and water or soil exposure, such as clearing brush, trekking, and gardening.

CLINICAL FINDINGS

• Incubation period is 2–30 days; most illnesses occur 5–14 days after exposure.
• Most infections are thought to be asymptomatic.
• Approximately 90% of clinical illnesses present as a nonspecific acute febrile illness, while approximately 10% progress to severe, potentially fatal illness with multi-organ dysfunction.
• Illness may be biphasic, with the patient briefly recovering from mild illness, but then developing more severe illness. 
• Symptoms can include fever, headache, myalgia (typically of the calves and lower back), conjunctival suffusion, nausea, vomiting, diarrhea, abdominal pain, cough, and sometimes a skin rash.
• Severe symptoms can include jaundice, renal failure, hemorrhage (especially pulmonary), aseptic meningitis, cardiac arrhythmias, pulmonary insufficiency, and hemodynamic collapse. Combined renal and liver failure associated with leptospirosis is referred to as Weil’s disease.
• Leptospirosis during pregnancy can cause fetal complications including fetal death or abortion.
• The case fatality rate for leptospirosis is approximately 5%–15% among patients with severe illness. Among patients with severe pulmonary hemorrhagic syndrome, the case fatality rate can exceed 50%.

TREATMENT

• Early treatment may decrease the severity and duration of disease. In patients with a high clinical suspicion of leptospirosis, initiating antibiotic treatment as soon as possible without waiting for laboratory results is recommended.
• For patients with mild symptoms, doxycycline is the drug of choice (100 mg orally, twice daily), if not contraindicated. Other options include azithromycin (500 mg orally, once daily), ampicillin (500-750 mg orally, every 6 hours), amoxicillin (500 mg orally, every 6 hours).
• For patients with severe disease, IV penicillin is the drug of choice (1.5 MU IV, every 6 hours), and ceftriaxone (1 g IV, every 24 hours) can be equally effective.

LABORATORY TESTING

• Antibodies for leptospirosis develop between 3-10 days after symptom onset, thus any serologic test must be interpreted accordingly – negative serologic test results from samples collected in the first week of illness do not rule out disease, and serologic testing should be repeated on a convalescent sample collected 7-14 days after the first.
•  In the acute phase of illness, leptospires are present in the blood (septicemia) for approximately the first 4–6 days of illness.
• Leptospires may be shed intermittently in the urine after approximately the first week of illness onset. Due to the transience of leptospires in body fluids, a negative PCR test does not rule out leptospisosis.
• It is best to submit as many specimen types as possible. Recommended specimens based on collection timing:
• Acute illness (first week): whole blood and serum
• Convalescent illness (after first week): serum +/- urine

PREVENTION

• The first line of leptospirosis prevention is to avoid exposure.
• Avoid wading, swimming, bathing, swallowing, or submersing head in potentially contaminated freshwater (rivers, streams) especially after periods of heavy rainfall or flooding.
• Avoid contact with floodwater, and do not eat food contaminated with floodwater.
• If exposure cannot be avoided, wear appropriate personal protective equipment (PPE) (rubber boots, waterproof coveralls/ clothing, gloves). Cover open wounds with waterproof dressings.
• Treat unsafe or potentially contaminated drinking water by boiling or chemically treating.
• Keep rodent populations (rats and mice) or other animal pests under control. Do not eat food that may have been exposed to rodents and possibly contaminated with their urine.
• Some studies have shown that chemoprophylaxis with doxycycline might be effective in preventing clinical disease and could be considered for people at high risk and with short-term exposures.

EBOLA VIRUS DISEASE

EBOLA VIRUS DISEASE

• Ebola Virus Disease (formerly known as Ebola haemorrhagic fever) is a severe, often fatal illness, with a death rate of up to 90%.
• The illness affects humans and nonhuman primates (monkeys, gorillas and chimpanzees)
• The disease was first identified in 1976 in two simultaneous outbreaks, one in a village near the Ebola River in the Democratic Republic of Congo, and the other in a remote area of Sudan.

THE INFECTIOUS AGENT

• A member of a family of RNA viruses called the Filoviridae
• Subtypes
• Ebola‐Zaire
• Ebola‐Sudan
• Ebola‐Ivory Coast
• Ebola‐Bundibugyo
• Ebola‐Reston.

TRANSMISSION

• Ebola virus occurs by handling of infected chimpanzees, gorillas and forest antelopes, both dead and alive.
• After the index case in an outbreak setting is infected, the virus can be transmitted in several ways.
•  Direct contact with blood and /or secretions of an infected person.
• Through contact with objects, such as needles, those have been contaminated with infected secretions.
• Burial ceremonies
• Nosocomial transmission 

INCUBATION PERIOD 

• The incubation period for Ebola HF ranges from 2 to 21 days

SYMPTOMS

CLINICAL DIAGNOSIS

Diagnosing Ebola HF during the first few days is difficult because of nonspecific early symptoms, such as red eyes and skin rash. However, if a person has the constellations of symptoms described above with corroborating epidemiological evidence, Ebola virus infection can be suspected.

LABORATORY DIAGNOSIS

• Early
• Serology [Antigen‐capture enzyme‐linked immunosorbent assay (ELISA) testing, IgM ELISA]
•  PCR
• virus isolation 
• Late
• IgM and IgG antibodies.
• Post
• humus Immuno‐histochemistry testing,
• Virus isolation
• PCR

LABORATORY FINDINGS

• Low white blood cell and platelet counts and elevated liver enzymes.
• Treatment
• There is no specific treatment for Ebola HF. Patients receive supportive therapy. This consists of balancing the patient’s fluids and electrolytes, blood pressure and treating them symptomatically and treating for any complicating infections.

PREVENTION

• Suspected cases should be isolated from other patients
• Inform MoH, Epidemiology Unit and RDHS immediately.
• All hospital staff should be briefed on the nature of the disease and its mode of transmission.
• Strict barrier nursing techniques should be implemented.
• Particular emphasis should be placed on ensuring that invasive procedures such as placing of intravenous lines and handling of blood, secretions, catheters and suction devices are carried out under strict barrier nursing conditions.
• Hospital staff should have individual gowns, gloves, masks, closed resistant shoes (e.g. boots) and goggles etc. Non‐disposable protective equipment must be reused only after they have been properly disinfected.
• Perform hand hygiene before and after direct patient care
• Infection may also spread through contact with soiled clothing or bed linen from a patient with Ebola. 
• Protective clothing should be worn when handling soiled linen and soiled linen should be disinfected with an effective disinfectant (e.g. 1% Sodium Hypochlorite Solution) in addition to the normal cleaning procedures. Contaminated surfaces should be disinfected with an effective disinfectant (e.g. 1% Sodium Hypochlorite Solution).
• Contacts Contact tracing and case finding interviews should be conducted outdoors whenever possible and a distance of more than one metre should be maintained between interviewer and interviewee. Protective equipment is not required if this distance is assured. Protective equipment is not required when interviewing asymptomatic individuals
• Burial of the deceased Post‐mortem examination of HF patient remains should be limited to essential evaluations only Remains should be wrapped in sealed, leak‐ proof material and should be buried promptly. Only trained personnel should handle the human remain

TETRALOGY OF FALLOT

TETRALOGY OF FALLOT

DEFINITION

•       Tetralogy of fallot (TOF) is a defect that consists of 4 pathologies which lead to obstruction of bloodflow to the lungs, causing cyanosis. The degree of cyanosis depends on the degree of pulmonary stenosis or atresia. The four pathologies include:

o  Pulmonary stenosis / pulmonary atresia

o Right ventricular hypertrophy

o Overriding aorta

o Ventricular septal defect

   

•        Tetralogy of fallot is classified into cyanotic and acyanotic.

o   Cyanotic: classic tetralogy of fallot is a cyanotic defect, and this is due to the degree of pulmonary stenosis. The greater the obstruction of the right ventricular outflow tract, the greater the degree of cyanosis, and the greater severity of symptoms.

o   Acyanotic: acyanotic tetralogy of fallot, also known as the “pink tet” is less common than the cyanotic type. The degree of pulmonary stenosis is not enough to cause persistent right to left shunting. Symptoms may include only mild cyanosis with agitation or exercise. However, signs of right heart damage can be seen without symptoms, and these include right ventricular hypertrophy, right ventricular and right atrial enlargement. This defect is usually closed before six months of age.

EPIDEMIOLOGY

•          Most common form of cyanotic heart disease.
•          1 in 4 will die before 12months of age if unrepaired
•          >50% chance of death by age 4 years if unrepaired

PATHOPHYSIOLOGY

•          An obstruction of blood flow to the lungs which causes hypoxia, cyanosis and enlargement if the right heart.
•          Events that cause an increase in pulmonary pressure, ie agitation, crying and bowel movements, contribute to an increase in pulmonary stenosis. The stenosis leads to further obstruction of blood flow to the lungs causing the classic hypoxic spell. The blood then shunts to the left side of the heart and returns to the body as deoxygenated blood.
•          The obstruction of blood flow to the lungs cause cyanosis, which can cause the classic hypoxic spell. Characteristics of hypoxic spell include the following:

o   Rapid and deep respiration

o   Irritability and prolonged crying

o   Increasing cyanosis

o   Decreased intensity of heart murmur

o   Loss of consciousness, seizure, stroke and death can occur if the spell is not relieved.

CLINICAL SIGNS AND SYMPTOMS

•          Acyanotic:

o   Mild pulmonary stenosis, Mild Left to right, asymptomatic “pink tet”

•         Cyanotic:

o   Moderate to severe pulmonary stenosis, right to lest shunting, symptomatic, “blue tet”

•        The severity of the following symptoms is directly dependent upon the severity of pulmonary stenosis (PS)

o   Clubbing

o   Cyanosis

o   Dyspnea on exertion

o   Shortness of breath

o   Exercise intolerance/easy fatigability.

o   Squatting

o   Systolic thrill, systolic ejection murmur at middle LSB

o   EKG: RAD, RVH

o   Chest X ray : “boot – shaped “heart, normal heart size

o   ECHO: anatomy, coronary arteries

o   CXR- TOF

 “boot – shaped “heart

Clubbing

MEDICAL MANAGEMENT

•          Medical management include management of the acute and chronic phases of the disease.
•          Chronic medical management:

o   Digoxin

o   Beta blockade (propranolol)

•          Acute medical management of cyanotic/ hypoxic spells

o   Calm the baby (place the baby in mother’s arms, feed, pacifier)

o   Knee/chest position: increases blood return to the heart and systemic vascular resistance (SVR) and forces blood flow into the lungs.

o   Oxygen: the most potent pulmonary vasodilator. Even though blood is shunting right to left, oxygen will decrease the pulmonary vascular resistance (PVR) and may shift the flow of blood to the lungs as the pulmonary resistance falls.

o   Morphine sulfate: reduces pulmonary vascular resistance (PVR)

o   Hyperpnea: reduces PVR

o   Phenylephrine

o   NaHCO₃  for acidosis

Knee/chest position

SURGICAL MANAGEMENT

•         BT Shunt

o   Is a palliative procedure that is performed to buy time until a complete repair can performed.

o   Provides secure unobstructed blood flow to the lungs.

o   Usually a 3mm, 3.5mm or 4.0mm gortex tube graft connecting the innominate artery to the pulmonary artery.

o   Is a non-cardiopulmonary bypass procedure.

o   Is sometimes used if the baby is very symptomatic, ie having cyanotic spells, and also weighs less than 3kg.

BT Shunt

•         Complete repair

o   Usually around 6 months of age, or sooner if symptomatic

o   The pulmonary stenosis is surgically relived.

o   The VSD is closed.

o   The overriding aorta is realigned during the closure of the VSD.

o   The right ventricular hypertrophy resolves over time.

POSTOPERATIVE MANAGEMENT AND NURSING IMPLICATIONS

•         Maximize CO – Inotropes, lusotropes, vasodilators, diuretics

o   Common inotropic continuous infusions may be epinephrine, dopamine, and milrinone.

•          Assess for residual VSD/RVOT obstruction

o   Evidenced by continued desaturation.

•         Arrhythmia:

o   Heart block: temporary external pacing

o   Jet: cooling , amiodarone, pacing

PATENT DUCTUS ARTERIOSUS (PDA)

PATENT DUCTUS ARTERIOSUS (PDA)

DEFINITION

• Fetal connection between aorta and pulmonary artery persist (PDA)

EPIDEMIOLOGY

• 5- 10% of all congenital heart disease.
• Increase incidence in premature infants.

PATHOPHYSIOLOGY

• Left to right shunt with left ventricular volume overload.

CLINICAL SIGNS AND SYMPTOMS

• Symptoms depend on the size of the PDA.
• Asymptomatic to congestive heart failure (particularly in preemies)
• Machinery type murmur best heart at the upper left sternal border
• Bounding pulses with wide pulse pressure (large defect)
• Echo confirm suspicion, determine size, location, pulmonary artery pressures
• EKG range from normal to left ventricular hypertrophy, right ventricular hypertrophy (depends on size of defect)
• Chest X ray normal to cardiomegaly with increase pulmonary vascular markings

Echo in PDA

MEDICAL MANAGEMENT

• Diuretics
• Ibuprofen

SURGICAL MANAGEMENT

• Ligation/ surgical clip: (L) thoracotomy or video assist thorascopic surgery
• Ductus occlusive device

VENTRICULAR SEPTAL DEFECT (VSD)

VENTRICULAR SEPTAL DEFECT (VSD)

       DEFINITION

• Abnormal communication between ventricles
• Left to right shunt
• The defect can occur anywhere in the ventricular septum and are classified into four types:
•   Supracrystal: below valve,associated with aortic valve insufficiency
•  Perimembranous
•  AV (atrioventricular) canal type
•  Muscular

      

 EPIDEMIOLOGY

• Most common form of congenital heart disease, 20 – 25%
• Spontaneous closure occur in 30% to 40% of all cases (usually in 1^st year of life)
• Males > females
• Associated with tetralogy of fallot, transposition of the great arteries, truncus arteriosus and coarctation of the aorta

  PATHOPHYSIOLOGY

• Left to right shunt
• Overcirulation of the pulmonary bed
• Right ventricular overload resulting in right ventricular hypertrophy

  CLINICAL SIGNS AND SYMPTOMS

• Congestive heart failure (CHF) in infants with large defects
• Grade 2 – 5/6 regurgitate systolic murmur at the left lower sternal border
• EKG: small VSD: normal; mod VSD: left ventricular hypertrophy, left atrial hypertrophy (LAH) . Large VSD: CHF, LAF (left atrial hypertrophy), biventricular hypertrophy
• Chest x-ray normal to cardiomegaly
• ECHO (echocardiogram) – determine size of defect, location, shunting, associated defects

  MEDICAL MANAGEMENT

• Digoxin
• Diuretics
• Nutritional support 

  SURGICAL MANAGEMENT

• Closure
•   Primary closure involves closure with sutures
•   Patch closure involves using a piece of the patient’s native pericardium or gortex patch
• Pulmonary artery banding
•   A band is placed around the pulmonary artery and limits the amount of blood flow to the lungs. This is a procedure that does not require cardiopulmonary bypass and May opted for when the patient is small for gestational age, or < 3kg 

          Surgical closure of VSD

Pulmonary artery banding