Archive | June 2011

Intramuscular (IM) Vaccine Injection (Age and Gauge)

Newborn (0–28 days)
  • Site: Anterolateral thigh muscle
  • Needle Gauge:  ⅝”* (22–25 gauge)
Infant (1–12 months)
  • Site: Anterolateral thigh muscle
  • Needle Gauge:  1″ (22–25 gauge)
Toddler (1–2 years)
  • Site: Anterolateral thigh muscle, 1–1¼” (22–25 gauge)
  • Site: Alternate site: Deltoid muscle of arm if
    muscle mass is adequate, ⅝–1"* (22–25 gauge)

Children (3–18 years)

  • Site: Anterolateral thigh muscle, 1–1¼” (22–25 gauge)
  • Site: Deltoid muscle (upper arm), ⅝–1″* (22–25 gauge)
Adults 19 years and older
  • Site: Anterolateral thigh muscle, 1–1½” (22–25 gauge)
  • Site: Deltoid muscle (upper arm), 1–1½”* (22–25 gauge)

Reference: BCCDC http://www.immunize.org/catg.d/p2020.pdf

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Chorionamnionitis

An infection of the chorion and amnion, the sacs surrounding the fetus in the womb.

Etiology:

  1. Group B streptotococcus
  2. bacterial vaginosis
  3. Ruptured membranes prolonged period of time
Clinical presentation:

clinical signs and symptoms of chorioamnionitis include the following:

  • Fever (an intrapartum temperature >100.4ºF or >37.8ºC)
  • Significant maternal tachycardia (>120 beats per minute [bpm])
    The fetus may also have tachycardia (>160-180 bpm).
  • Fetal tachycardia (>160-180 bpm)
  • Purulent or foul-smelling amniotic fluid or vaginal discharge
  • Uterine tenderness
  • Maternal leukocytosis (total blood leukocyte count >15,000-18,000 cells/μL)
Prognosis:
Infants born to mothers with chorioamnionitis have unfavorable neurologic outcomes. Cerebral palsy and cognitive impairment without CP have a relationship to the presence of maternal chorioamnionitis. Functional polymorphism in the cytokine interleukin (IL)-6 gene is a risk factor for CP.
Treatment and management:
Treatment of infections such as vaginosis during pregnancy and antibiotic treatment of those with rupture membranes for a prolonged period of time.

Haemolytic-uraemic syndrome

Haemolytic-uraemic syndrome (HUS) is primarily a disease of infancy and early childhood and is classically characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure.

Microbiology:

Haemolytic uraemic syndrome is part of a disease category known as  thrombotic microangiopathies.

Pathophysiology:

Haemolytic uraemic syndrome is characterized by the involvement of widespread occlusive microvascular thromboses resulting in thrombocytopenia, microangiopathic hemolytic anemia, and variable signs and symptoms of end-organ ischemia.

After entering the circulation via the gastrointestinal mucosa, the toxin preferentially localizes to the kidneys, inhibiting protein synthesis and eventually leading to cell necrosis or apoptosis. Endothelial cell damage subsequently potentiates renal microvascular thrombosis by promoting activation of the blood coagulation cascade. Platelet aggregation results in a consumptive thrombocytopenia. Microangiopathic hemolytic anemia results from mechanical damage to red blood cells circulating through partially occluded microcirculation.

Etiology:

E coli serotype O157:H7 has been associated with more than 80% of infections leading to hemolytic uremic syndrome.

The new E. coli variant of the rare strain O104 out of Germany is the cause of a new European outbreak.

E. coli O104’s present strain variant posesses a gene which produces a toxin and another which helps the bacterium colonise the gut more efficiently, which effectively means even more toxin is produced.