Decreased Activity Level - Case 2-4: 11-Month-Old Boy
Decreased Activity Level - Case 2-4: 11-Month-Old Boy: Excerpt from Pediatric Complaints and Diagnostic Dilemmas
I. History of Present Illness
An 11-month old boy was brought to the emergency department because of decreased
activity level. He had had a 3-day illness consisting of fever to 39
°C and diarrhea. He had had approximately four episodes of nonbloody diarrhea per
day. He had no history of emesis. On the day of presentation, he had been tired
all day and wanted to lie down constantly. He had consumed four 8-ounce bottles
of Pedialyte. His urine output was decreased. The mother called the paramedics
when she felt that he was worsening.
II. Past Medical History
His prenatal and birth histories were normal. He had a history of wheezing, with
an upper respiratory tract infection at 3 months of age. He had had no
hospitalizations or surgeries. He was taking no medications and had no
allergies. His immunizations were current.
III. Physical Examination
T, 40.3°C; RR, 46/min; HR, 183 bpm; BP, 99/41 mm Hg
Weight and height, 75th percentile
On examination, he was lethargic and minimally responsive to painful stimuli.
The head and neck examination did not reveal any signs of external trauma. His
gaze was dysconjugate, but pupils were reactive from 3 mm to 2 mm bilaterally.
He had sunken eyes and dry mucous membranes. Respiratory examination revealed
shallow, labored respirations with moderately increased work of breathing. He
had intercostal and substernal retractions as well as abdominal breathing.
Breath sounds were coarse to auscultation. Cardiac examination was significant
for the tachycardia; there was no murmur or abnormal cardiac sounds. Abdominal
examination revealed hypoactive bowel sounds but no tenderness or
hepatosplenomegaly. There were no masses. Rectal examination revealed gross
blood. Neurologic examination was significant for overall hyoptonia and
unresponsiveness. Cranial nerves were intact and deep tendon reflexes were 2+
and symmetric. He had an intact gag reflex.
IV. Diagnostic Studies
In the emergency department, blood, urine, and CSF cultures were obtained.
Additional laboratory studies revealed a WBC count of 13,400 cells/mm
3, with 11% bands, 63% segmented neutrophils, 34% lymphocytes, and 2% monocytes.
Hemoglobin was 6.6 g/dL; platelets, 195,000/mm
3; sodium, 131 mmol/L; potassium, 5.8 mmol/L; chloride, 101 mmol/L; carbon
dioxide, 18 mmol/L; blood urea nitrogen, 19 mg/dL; creatinine, 0.7 mg/dL; and
glucose, 57 mg/dL. His prothrombin time (PT) was prolonged at 16.4 seconds, and
his activated partial thromboplastin time (PTT) was 29.1 seconds. Serum and
urine toxicology screens were negative.
V. Course of Illness
Immediate, life-threatening causes were initially addressed. Coffee-ground
material was aspirated from the stomach after placement of a nasogastric tube.
Pediatric surgery staff were consulted in the emergency department on suspicion
of an intraabdominal catastrophe, particularly intussusception or volvulus. He
received broad-spectrum antimicrobial agents and was immediately taken to the
operating room for an exploratory laparotomy. In the intensive care unit, after
the procedure, the patient developed a rash that suggested the diagnosis (Fig.
2-2).
Discussion: Case 2-4
I. Differential Diagnosis
This child's critical appearance, in association with fever, made the clinician most
concerned for an overwhelming systemic infection. The original source could
have been a bacterial infection such as bacteremia, pneumonia, pyelonephritis,
or meningitis. Aside from infectious causes, the history of bright red blood
from the rectum is concerning for intestinal ischemia. Intussusception,
malrotation with volvulus, or some other abdominal catastrophe could result in
a similar clinical picture at presentation. Other causes of bleeding diathesis
should be considered as well.
II. Diagnosis
Because of the concern for an abdominal catastrophe, the child was taken to the
operating room for an exploratory laparotomy. The laparotomy findings were
normal; there was no volvulus or intussusception. While the child was in the
operating room, an alert laboratory technician noted gram-negative
intracellular diplococci on the peripheral blood smear. In the intensive care
unit, the patient developed diffuse purpuric lesions that suggested bacterial
sepsis due to
Neisseria meningitidis (see Fig. 2-2). His blood and CSF cultures ultimately grew N. meningitidis. The diagnosis is meningococcal meningitis and sepsis.
III. Incidence and Epidemiology
N. meningitidis (meningococcus) is a gram-negative diplococcus. It causes bacteremia and
meningitis. There are 13 serogroups, but serogroups A, B, C, Y, and W-135 are
most frequently implicated in the United States. Serogroups B, C, and Y each
account for about 30% of systemic disease.
N. meningitidis is a component of the normal flora of the upper respiratory tract, which is the
only reservoir for the organism. Transmission occurs via respiratory secretions
and by person-to-person contact. Approximately 2.5% of children and 10% of the
general population are asymptomatic carriers. In one study, 32.7% of persons
between the ages of 20 and 24 years were found to be asymptomatic carriers.
Peak rates of infection occur between November and March. The incubation period
is most commonly less than 4 days but can be as long as 10 days. Fifty percent
of cases of meningococcemia occur in children younger than 2 years of age;
however, during epidemics, there is a shift in incidence toward older children,
adolescents, and young adults.
IV. Clinical Presentation
The disease caused by N. meningitidis varies from asymptomatic transient bacteremia to fulminant sepsis and death.
Pathogenic
N. meningitidis colonizes the respiratory tract and may invade the bloodstream. The patient
becomes bacteremic and progressively sicker. The bacteremia may seed the
meninges, causing meningitis. Those patients who present with meningitis have a
better prognosis than do patients with bacteremia alone. Shortly after the
administration of appropriate antibiotics, some patients have a marked clinical
deterioration, ranging from hypotension to death. This deterioration is thought
to be caused by stimulation of the host inflammatory pathway by endotoxin (a
component of the gram-negative bacterial cell wall). Meningococcal disease can
lead to death in as few as 12 hours. Invasive infection usually results in
meningococcemia, meningitis, or both. However, the bacteria can infect any
organ, including myocardium, adrenals, lungs, and joint spaces. Approximately
55% of patients with meningococcal disease have meningitis. Additionally, 50%
of patients have positive blood cultures.
A history of a preceding upper respiratory tract infection can often be elicited
from patients with meningococcemia. The onset of illness is abrupt, with fever,
lethargy, and rash. The rash is typically petechial and occasionally urticarial
or maculopapular. Some patients develop fulminant meningococcemia, with
disseminated intravascular coagulopathy, shock, and myocardial dysfunction.
Coagulopathy leads to the development of purpura. There is a 20% mortality rate
in cases of fulminant disease.
V. Diagnostic Approach
The prompt diagnosis of meningococcal disease requires a high index of clinical
suspicion. Recovery of the organism from a normally sterile site provides the
definitive diagnosis.
Appropriate cultures. The organism can be isolated from blood, CSF, and scrapings from the petechial
rash. Blood cultures are positive in about 50% of patients with presumed
meningococcal disease. Because the organism is a normal component of the
nasopharynx, nasopharyngeal cultures are not helpful.
Other studies. Children with meningococcemia are often critically ill. Laboratory studies that
may affect management include serum electrolytes, PT, and PTT.
VI. Treatment
The initial antimicrobial coverage of meningococcal infections should be a
third-generation cephalosporin such as cefotaxime or ceftriaxone.
Chloramphenicol, although rarely used, is appropriate for patients who have
anaphylactoid reactions to penicillins or cephalosporins. Although most
isolates in the United States are sensitive to penicillin, penicillin-resistant
isolates, first identified in Spain in 1987, are prevalent in Spain, Italy, and
parts of Africa. In the United States, routine susceptibility testing is not
indicated. Therapy for 5 to 7 days is adequate for most cases of invasive
meningococcal disease. There does not appear to be a role for steroid use.
Treatment with heparin and other anticoagulants remains controversial.
Chemoprophylaxis is indicated for individuals who were exposed to the index case
within 7 days before the onset of illness. Particularly, all household
contacts, all daycare or nursery school contacts (children and adults), and
health care workers who had intimate exposure to secretions (e.g.,
mouth-to-mouth resuscitation, secretions that came in contact with the health
care worker
's mucous membranes) should be treated prophylactically. Family members of the
index case have a 400 to 800 times higher risk for invasive disease. If the
index patient received only penicillin for therapy, then the patient should
also be treated with chemoprophylaxis to eradicate the organism. School age
classmates do not need chemoprophylaxis because they are not at increased risk
of disease. The drug of choice for chemoprophylaxis is rifampin, but
ceftriaxone (intravenous or intramuscular) and single-dose ciprofloxacin or
azithromycin are reasonable alternatives. All cases must be reported to the
local public health department.
Additionally, a polysaccharide vaccine that is effective against serogroups A,
C, Y, and W-135 is available. This vaccine should be routinely administered to
children who are functionally or anatomically asplenic, children who have
terminal complement deficiencies, college students living in the dormitories,
and military recruits. A conjugate meningococcal vaccine is being evaluated in
clinical trials.
VII. References
1. American Academy of Pediatrics. Meningococcal infections. In: Pickering LK,
ed.
2000 Red Book: Report of the Committee on Infectious Diseases, 25th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2000:396–401.
2. Anderson MS, Glode MP, Smith AL. Meningococcal disease. In: Feigin RD,
Cherry JD, eds.
Textbook of pediatric infectious diseases, 4th ed. Philadelphia: WB Saunders, 1998:1143–1156.
3. Cohen J. Meningococcal disease as a model to evaluate novel anti-sepsis
strategies.
Crit Care Med 2000;28:s64–s67.
4. Herf C, Nichols J, Fruk S, et al. Meningococcal disease: recognition,
treatment, and prevention.
The Nurse Practitioner 1998;23:30–46.
5. Kirsch EA, Barton RP, Kitchen L, et al. Pathophysiology, treatment and
outcome of meningococcemia: a review and recent experience.
Pediatr Infect Dis J 1996;15:967–979.
6. Periappuram M, Taylor M, Keane C. Rapid detection of meningococci from
petechiae in acute meningococcal infection.
J Infect 1995;31:201–203.
7. Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med 2001;344:1378–1388.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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