Vomiting - Case 3-1: 7-Week-Old Boy
I. History of Present Illness
A 7-week-old African-American male infant presented with a 2-day history of
frequent vomiting. The vomiting was nonprojectile, nonbilious, and, on one
occasion, streaked with blood. Oral intake was poor. He had urinated once over
an 18-hour period. On the day of admission, he had profuse, watery diarrhea. No
one in the family had had vomiting or diarrhea.
II. Past Medical History
The patient was born at term and weighed 3,300 g. He was delivered via cesarean
section due to arrested descent. Because of feeding difficulties in the
nursery, he was discharged home on a lactose-free formula. Since then, his oral
intake had been appropriate. He had not previously been hospitalized. He had
received his first hepatitis B immunization.
III. Physical Examination
T, 38.1°C; RR, 50/min; HR, 170 bpm; BP, 86/38 mm Hg; SpO2, 88% in room air
Weight, 4.0 kg (10th percentile); length, 25th percentile; head circumference,
10th percentile
Examination revealed a well-nourished infant who was crying but consolable (Fig.
3-1).
The anterior fontanelle was open and slightly sunken. The mucous membranes were
moist, and the sclerae were nonicteric. The lungs were clear to auscultation,
and the cardiac examination was normal without any murmurs. The abdomen was
soft and mildly distended, without hepatomegaly or splenomegaly. The
extremities were cool. He had no rashes, good tone, and a symmetric neurologic
examination.
IV. Diagnostic Studies
Laboratory evaluation revealed 24,500 white blood cells(WBCs)/mm3, with 9% band forms, 24% segmented neutrophils, 40% lymphocytes, 20% monocytes,
and 5% atypical lymphocytes. The hemoglobin was 15.2 g/dL, and the platelet
count was 577,000 cells/mm
3. On red blood cell morphologic analysis, mild anisocytosis, poikilocytosis, and
burr cells were noted. Serum chemistries and cerebral spinal fluid analysis
were normal. His urine was dark yellow and turbid, with a specific gravity of
1.038, a pH of 5.5, 3+ protein, and 5 to 10 granular casts without bacteria,
nitrites, or WBCs. On chest radiography, the cardiac silhouette and lung fields
were normal.
V. Course of Illness
The patient's oxygen saturation on pulse oximeter increased to 93% when oxygen was
administered by nasal cannula. Four extremity blood pressures were obtained as
follows: right arm, 90/32 mm Hg; left arm, 88/42 mm Hg; right leg, 80/40 mm Hg;
left leg, 76/35 mm Hg. On arterial blood gas (ABG) analysis, the pH was 7.01;
partial pressure of carbon dioxide (PaCO
2), 18 mm Hg; partial pressure of oxygen (PaO2), 232 mm Hg; bicarbonate level, 4.7 mEq/L; and base deficit, 24.7. The patient
received multiple normal saline boluses and bicarbonate in an attempt to
correct his metabolic acidosis. The appearance of the patient (see Fig. 3-1) in
conjunction with the ABG results suggested a diagnosis.
Discussion: Case 3-1
I. Differential Diagnosis
Vomiting in early infancy can be a very worrisome symptom. The most common cause
of emesis in this age group is GER, either physiologic or due to overfeeding.
Anatomic obstruction should always be considered. Obstructive lesions include
malrotation with a volvulus, intestinal or esophageal atresia, pyloric
stenosis, congenital adhesions or bands, incarcerated hernia, intussusception,
and Hirschsprung
's disease. The level of the obstruction determines whether the vomitus is
bilious and whether the abdomen is distended. Infectious causes include
gastroenteritis, urinary tract infection, meningitis, pneumonia, and
pericarditis. Bloody streaks in the emesis could be the result of a milk
protein allergy, gastroenteritis, necrotizing enterocolitis, or achalasia.
Metabolic disorders must be considered in this child who presents with vomiting
and a significant metabolic acidosis. Etiologies such as congenital adrenal
hyperplasia (CAH), adrenal hypoplasia, inborn errors of metabolism including
both amino acid and organic acid disorders, and galactosemia must also be
considered.
II. Diagnosis
The patient was cyanotic, a feature best visualized by noting the contrast of
his lips with the white portion of the blanket (see Fig. 3-1). An ABG analysis
with co-oximetry measurements revealed acidosis, with a pH of 7.01; PaCO
2, 18 mm Hg; and PaO2, 232 mm Hg. Co-oximetry readings revealed an oxyhemoglobin of 78.2%; methemoglobin, 21.8%;
and lactate, 2.7 mmol/L, confirming the diagnosis of methemoglobinemia.
III. Incidence and Epidemiology of Methemoglobinemia
Although methemoglobinemia is a rare condition in pediatrics, it can cause
significant cyanosis and even death. Methemoglobin is a derivative of normal
hemoglobin in which the iron component has been oxidized from the ferrous (Fe
2+) to the ferric (Fe3+) state. The oxidized iron (Fe3+) is unable to reversibly bind oxygen. Therefore, the oxidation of hemoglobin to
methemoglobin produces a functional anemia by impairing the ability of the
blood to transport oxygen. Methemoglobin occurs regularly in the body but
rarely exceeds levels of 2% of the total hemoglobin because of antioxidant
reactions in the body that reduce methemoglobin back to hemoglobin. The most
important of these antioxidant reactions uses either reduced nicotinamide
adenine dinucleotide (NADH)
–cytochrome b5 reductase or NADH phosphate (NADPH)–methemoglobin reductase. NADPH-methemoglobin reductase also reduces methylene
blue, an action that has important therapeutic implications, as described in
the treatment section below.
Methemoglobin levels increase when there is a disturbance in the balance between
the oxidation and reduction of heme iron. Infants are at an increased risk for
methemoglobinemia for two main reasons: (a) young infants have a lower level of
the reductase enzymes, and (b) fetal hemoglobin is more easily oxidized than
adult hemoglobin. Methemoglobinemia can be caused by exposure to oxidant drugs,
development of acidosis, or inherited conditions. The most common oxidizing
agents in acquired methemoglobinemia are sulfonamides, aniline dyes, chlorates,
quinones, benzocaine, lidocaine, metoclopramide, and phenytoin. Ingestion of
well water nitrates can also cause methemoglobinemia. Gastroenteritis with
acidosis can cause methemoglobinemia in infants, especially when
nitrite-forming bacteria such as
Escherichia coli and Campylobacter jejuni are present. Less common causes are inherited deficiencies of erythrocyte
methemoglobin reductase or the presence of M hemoglobin.
IV. Clinical Presentation
The clinical presentation of patients with methemoglobinemia depends on the
serum concentrations of both hemoglobin and methemoglobin. Increasing
methemoglobin levels are associated with progressively worsening symptoms.
Patients with lower serum hemoglobin concentrations are affected at lower
levels of methemoglobin. Patients with methemoglobin concentrations lower than
10% rarely have symptoms unless they are already anemic. Most patients with
concentrations of methemoglobin between 10% and 25% have cyanosis but few other
symptoms. Depending on the degree of cyanosis, metabolic acidosis may also
develop. Levels from 30% to 50% are associated with confusion, dizziness,
fatigue, headache, tachypnea, and tachycardia. Levels greater than 50% are
associated with severe acidosis, arrhythmias, seizures, lethargy, and coma.
Lethal levels occur at methemoglobin concentrations of about 70%.
V. Diagnostic Approach
Diagnosis of a rare pediatric condition like methemoglobinemia depends on having
a high index of suspicion. Clinical clues include a cyanotic child without
evidence of cardiac or pulmonary disease.
Bedside examination of blood. In a cyanotic patient, differentiating methemoglobin from deoxyhemoglobin is
important. On white filter paper, blood containing a high level of
methemoglobin turns chocolate brown; blood containing deoxygenated hemoglobin
appears dark red or purple initially but turns bright red on exposure to
atmospheric oxygen.
Potassium cyanide test. This test distinguishes between methemoglobin and sulfhemoglobin. Methemoglobin
reacts with cyanide to form cyanomethemoglobin. The formation of
cyanomethemoglobin turns the blood from chocolate brown to bright red.
Sulfhemoglobin appears dark brown initially and does not change color after the
addition of potassium cyanide.
Pulse oximetry. Oxygen saturation, as measured by pulse oximetry, is falsely elevated in the
presence of methemoglobinemia. By using two wavelengths of light, the pulse
oximeter determines
“functional oxygen saturation,” which is the ratio of oxyhemoglobin to all hemoglobin capable of carrying
oxygen. Normally, all hemoglobin present can potentially carry oxygen, so that
functional and true oxygen saturation are equal. Because methemoglobin does not carry oxygen, it
does not register as functional hemoglobin on the pulse oximeter. At normal
methemoglobin levels (less than 2%), this exclusion is not important, but at
high methemoglobin levels (greater than 10%), the functional and true oxygen
saturations differ substantially. Pulse oximeter readings may be abnormal with
methemoglobinemia. Because of the light absorption characteristics of
methemoglobin, the pulse oximetry readings will not drop below 82% unless there
is an accompanying increased level of deoxyhemoglobin.
Arterial blood gases. Children with methemoglobinemia have a normal or an abnormally elevated PaO2, as calculated by a blood analyzer, in the presence of cyanosis. PaO2 refers to dissolved oxygen molecules, not oxygen molecules bound to hemoglobin. In ABG measurements, the PaO2 is a value that is calculated from the measured pH and PaCO2 values. The calculation of PaO2 is based on the assumption that the hemoglobin function is normal. A
dyshemoglobin such as methemoglobin cannot carry oxygen but does not interfere
with pulmonary oxygen diffusion. Therefore, the PaO
2 calculated by the blood gas analyzer is falsely elevated.
Co-oximetry. Co-oximeters are spectrophotometers that measure light absorbance at different
wavelengths, including the wavelengths for methemoglobin, oxyhemoglobin,
deoxyhemoglobin, and carboxyhemoglobin. Co-oximeters accurately distinguish
methemoglobin from oxyhemoglobin and provide a definitive diagnosis.
Interpretation of results from a blood gas analyzer without co-oximetry may
lead to misdiagnosis, because the blood gas analyzer calculates the PaO
2 and the co-oximeter measures it directly.
VI. Treatment
Treatment regimens for methemoglobinemia depend on the level and the patient's symptoms. In general, only symptomatic patients with methemoglobin levels
greater than 20% or asymptomatic patients with methemoglobin levels greater
than 30% require specific therapy. Patients with concurrent problems that
impair oxygen delivery, such as anemia, cardiac disease, or pulmonary disease,
should be treated even if they have low methemoglobin levels. Symptomatic
patients must receive proper airway management and supplemental oxygen as
needed. Intravenous methylene blue, after reduction to leukomethylene blue by
NADPH-methemoglobin reductase, aids in the reduction of methemoglobin back to
hemoglobin. It is the treatment of choice and should reduce methemoglobin
levels significantly within 1 hour after administration. Exchange transfusions
are necessary for those patients who have extremely high levels of
methemoglobin that do not respond to methylene blue therapy.
Glucose-6-phosphate dehydrogenase (G6PD) is the first enzyme in the hexose
monophosphate shunt, which is the sole source of NADPH in the red blood cell.
Patients with G6PD deficiency may not produce sufficient NADPH to reduce
methylene blue to leukomethylene blue. Therefore, methylene blue therapy may
not be effective in patients with G6PD deficiency. In such patients, methylene
blue may also induce hemolysis.
VII. References
1. Lukens J. Methemoglobinemia and other disorders accompanied by cyanosis. In:
Lee RG, Foerster J, Lukens J, et al., eds.
Wintrobe's clinical hematology, 10th ed. Baltimore: Williams & Wilkins, 1998:1046–1055.
2. Pollack ES, Pollack CV. Incidence of subclinical methemoglobinemia in
infants with diarrhea.
Ann Emerg Med 1994;24:652–-656.
3. Ralston AC, Webb RK, Runciman WB. Potential errors in pulse oximetry:
effects of interference, dyes, dyshemoglobins and other pigments.
Anaesthesia 1991;46:291–294.
4. Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology,
and clinical management.
Ann Emerg Med 1999;34:646–656.
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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Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2008 Williams & Wilkins.
More About Causes of Vomiting
» Next page: Vomiting - Case 3-2: 9-Month-Old Girl (Pediatric Complaints and Diagnostic Dilemmas)
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