A 7-month old male infant arrived in the E.D. at 7:45 
a.m. after passing a dark maroon colored stool with 
clots at 7:00 a.m.  He has passed small amounts of 
blood in his stools intermittently since 4 months of age, 
but this current episode is the worst it has ever been.  
He has been taking amoxicillin-clavulinic acid for the 
past 7 days for otitis media.  He also has some nasal 
congestion and coughing.  He passed a normal stool at 
4:00 a.m. earlier.
     His past medical history is unremarkable except for 
the intermittent blood in his stool (small amounts).  
Stool cultures and examinations for ova and parasites 
done in the past as an outpatient were negative.  His 
growth has been good.  His development has been 
normal.  His diet consists of soy formula, baby foods, 
and table foods.
     Exam VS T37.0 (tympanic), P192, R40, BP 
154/128, oxygen saturation 94-95% in room air.  Alert, 
crying, in no distress.  Skin warm and dry.  Color pink.  
Anterior fontanelle soft and flat.  Pupils reactive.  TM's 
normal.  Oral mucosa moist.  Throat clear.  Neck 
supple.  Heart tachycardic, regular, without murmurs.  
Lungs good aeration, clear.  Abdomen soft, slightly 
distended, non-tender, bowel sounds active, no 
masses, no hepatosplenomegaly.  Peripheral pulses 
good.  Capillary refill time 2 seconds.  Excoriation noted 
over the perianal region.  Muscle tone good.  Moves all 
extremities well.  Stool is guaiac positive.
     Laboratory studies:  CBC WBC 10,900, 11 bands, 
32 segs, 51 lymphs, 2 monos, 3 eos, Hgb 11.4, Hct 
34.6, platelet count 176,000.  Prothrombin time and 
partial thromboplastin times are normal.  Urinalysis 
specific gravity 1.020, pH 6, 3-5 WBC's and 3-5 RBC's 
per high power field.  An IV is started and a clot tube for 
blood type and screening for possible transfusion is 
sent to the lab.  An abdominal series is ordered.

View Abdominal Series:  Flat (supine) view.


View Abdominal Series:  Upright view.

     His repeat vital signs at 8:35 a.m. show P172, R40, 
BP 141/100.  He passes two more bloody stools in the 
E.D. which appear to resemble currant jelly (blood 
mixed with mucus somewhat resembling strawberry 
jelly without the seeds).  A nasogastric tube is placed.  
An aspirate of his gastric contents is guaiac negative.  
At 9:40 a.m. his blood pressure falls.  He passes more 
blood per rectum.  He is transfused with packed RBC's.  
After stabilization, a water soluble contrast enema is 
performed to rule out intussusception.  This study is 
negative.
     In reviewing his abdominal series, the abdomen 
portion of the study is non specific.  However, the chest 
portion of the upright abdomen is positive for interstitial 
infiltrates.  In retrospectively reviewing his vital signs, 
his oxygen saturation of 94-95% in room air before he 
developed hemodynamic decompensation is suggestive 
of a significant ventilation perfusion mismatch 
suggesting some type of pulmonary condition.  Reactive 
airway disease is the most common cause of this, but 
since wheezing was not noted on examination, an 
occult pneumonia should be suspected.  Most infants 
with normal lungs should have an oxygen saturation of 
98-100% in room air.  This is especially true of young 
infants less than 3 months of age who almost always 
have an oxygen saturation of 100% in room air.  
Anything less than 98% should be viewed with some 
suspicion in this age group.  
     This interstitial pneumonia was appreciated in the 
E.D., however, the oxygen saturation rose to 100% with 
some blowby oxygen.  The hemodynamic stabilization 
seemed to have a greater  priority at the time.
     After stabilization in the intensive care unit, he was 
placed on cimetadine and IV fluids.  A Meckel's 
diverticulum was suspected.  His pneumonia was felt to 
be viral in etiology and he was not placed on any 
antibiotics.  His oxygen saturation stabilized at 99% with 
1 liter per minute of oxygen by nasal cannula. 
     After multiple consultants became involved in his 
care, he was started on antibiotics.  A nuclear medicine 
Meckel's scan was negative.  Endoscopy and 
colonoscopy were both negative.  He continued to 
bleed intermittently, requiring additional transfusions of 
RBC's and platelets.  Stool, blood, and urine cultures 
were negative.  He underwent an exploratory 
laparotomy.  Frozen section examination of intestinal 
biopsies were positive for viral inclusion bodies, 
suggesting cytomegalovirus enteritis.
     Probable severe CMV infection and the interstitial 
pneumonia raised the possibility of HIV infection.  His 
mother was not known to be HIV positive nor at high 
risk for HIV.  An HIV ELISA study was positive and an 
HIV p24 antigen assay was also positive.  He 
underwent extensive treatment with gamma globulin, 
anti-viral agents, antibiotics, and intensive care support.  
He eventually developed respiratory insufficiency and 
expired 15 days after presenting to the E.D.


     The classification of HIV is very detailed ranging 
from asymptomatic HIV infection to AIDS associated 
manifestations including specific secondary infections, 
recurrent serious bacterial infections, progressive 
neurologic disease, lymphoid interstitial pneumonitis, 
specific secondary malignancies (lymphomas and 
Kaposi sarcoma), and HIV wasting syndrome.  The 
details of this classification are beyond the scope of this 
case.
      Manifestations of HIV infection in children are 
extensive.  They are summarized here briefly by organ 
system.  Systemic manifestations include failure to 
thrive and recurrent or chronic fever.  The failure to 
thrive is usually due to reduced caloric intake secondary 
to anorexia and acclerated energy expended in fighting 
chronic infection.  Examination findings include 
hepatosplenomegaly, lymphadenopathy, and dermatitis.
     Cardiac manifestations are rarely the presenting 
finding in a new patient.  Cardiomyopathy, conduction 
abnormalities, and congestive heart failure may result 
directly from HIV or from other opportunistic viral 
infections.
     Pulmonary manifestations can be categorized as 
infectious and non-infectious.  Recurrent bacterial 
pneumonia, pneumocystis carinii pneumonia (PCP), 
viral pneumonia (including CMV), mycobacterium avium 
complex infections, and mycobacterium tuberculosis 
are some of the common pulmonary infections.  
Tuberculosis infections are often highly drug-resistant.  
Pneumocystis carinii pneumonia (PCP) is a diffuse, 
desquamative, interstitial infection resulting in 
hypoxemia, fever, productive cough, respiratory 
distress, and poor exercise tolerance.  PCP and 
Mycobacterium avium complex disease are two of the 
more severe infections affecting the later stages of HIV 
infection.
     Reactive airway disease is common among all 
immunocompromised children, probably due to chronic 
airway inflammation due to recurrent or chronic 
infections.  Lymphoid interstitial pneumonitis is the most 
common noninfectious pulmonary condition seen in 
pediatric HIV infection.  This is characterized by diffuse 
interstitial infiltrates.  Pulmonary fibrosis is also seen 
with HIV.  Children with advanced HIV 
encephalopathies may develop aspiration pneumonia.
     GI manifestations include candida esophagitis, CMV 
esophagitis, salmonellosis, shigellosis, 
campylobacteriosis, rotavirus gastroenteritis, etc.  
These infections are usually more severe than in 
non-HIV children.   Mycobacterium avium complex, 
cryptosporidium, CMV, and other viruses may all induce 
opportunistic enteropathies.  Clostridium difficile 
(pseudomembranous) colitis may develop in any patient 
treated with broad spectrum antibiotics for long periods 
of time.  HIV children are at risk of developing chronic 
hepatitis due to CMV or hepatitis B virus.  CMV and 
microsporidiosis have been identified as causes of 
biliary tract infection.  Pancreatitis may be caused by 
CMV or drug toxicity (pentamidine, didanosine, 
zalcitabine).
     Neurological manifestations result from progressive 
encephalopathy and retarded CNS development.  
There is progressive motor dysfunction and loss of 
developmental milestones.  Exam findings include 
weakness, flaccidity, hyperreflexia, spasticity, and gait 
abnormalities.  Seizures, cerebrovascular accidents, 
CNS lymphoma, and meningitis may also develop.  
Children may do well for several years.  Behavioral 
changes associated with chronic disease, interaction 
with peers, or frequent medical visits may mimic 
neurologic changes.  Zoster and varicella infections can 
be severe.
     Eye manifestions include frequent conjunctivitis and 
blepharitis.  Severe retinopathies are uncommon.  ENT 
manifestations include chronic otitis media and sinusitis.  
Eradication of these infections may be difficult.  These 
children are at risk of developing mastoiditis.  Tonsillar 
and adenoidal hypertrophy may result along with 
generalized lymphatic hypertrophy.  Oral infections 
include thrush, periodontitis, severe dental caries, 
parotitis, and cervical lymphadenopathy.
     Renal manifestations include nephrosis and 
recurrent urinary tract infections.  Children with HIV 
often manifest short stature and delayed puberty.  
Myopathies and non-specific rheumatologic conditions 
may develop.
     Anemia, granulocytopenia, lymphopenia, and 
thrombocytopenia all occur frequently with HIV.  
Lymphopenia is a later manifestation of progressive 
immune deficiency.  Patients may often present with 
findings similar to ITP (idiopathic thrombocytopenic 
purpura) or aplastic anemia.  Therapeutic agents such 
as trimethoprim-sulfamethoxasole, zidovudine, and 
conventional antibiotics may add to bone marrow 
depression.  Acquired circulating anticoagulants result 
in prolonged coagulation times.  Lymphomas occur in 
3% of patients.  Children are less susceptible to 
Kaposi's sarcoma.  
     Making the diagnosis of HIV infection in young 
children can be very difficult.  ELISA and Western blot 
assays detecting anti-HIV IgG antibody are highly 
sensitive and specific when used in adults.  However, 
these assays are often falsely positive in young children 
due to the detection of maternal antibodies in the 
infant's serum which can be detectable for as long as 
18 months after birth.  Only about 13% to 39% of 
babies born to HIV-infected mothers will develop HIV 
infection.  Although overly sensitive in infants, these 
commonly used tests are able to identify infants at risk 
of developing HIV infection by identifying infected 
mothers.
     More specific tests for young children include in vitro 
production of HIV-specific antibodies by the child's 
lymphocytes, detection of IgA anti-HIV antibodies, 
detection of HIV p24 antigen (after decomplexing HIV 
antigen-antibody complexes), HIV culture, and 
polymerase chain reaction for detection of HIV-specific 
nucleic acid sequences.  However, these tests are not 
as widely available.
     As this case points out, any patient could be 
potentially infected with HIV.  Universal precautions 
should be practiced routinely to prevent occupational 
and nosocomial transmission.  The child in this case 
came from a low risk family residing in a low risk 
community.  In contrast to hospital personnel working in 
a high risk community who routinely practice universal 
precautions, hospital personnel in low risk settings may 
actually be at higher risk by not practicing universal 
precautions routinely.

References
     Church JA.  Clinical Aspects of HIV Infection in 
Children.  Pediatric Annals 1993;22(7):417-427.
     Church JA.  The Diagnostic Challenge of the Child 
Born At Risk For HIV Infection.  Pediatric Clinics of 
North America 1994;41(4):715-725.