History And Physical Examination Findings That Should Raise Suspicion For CHD In An Infant Or Child With Tachypnea, Cyanosis, And/Or Shock

History of poor feeding for several days to weeks preceding illness: Less than 3 ounces or greater than 40 minutes per feed or poor weight gain

 

Absence of fever in history or in ED: Temperature less than 38.3°C (100.4°F)

 

Upper extremity hypertension or decreased lower extremity blood pressure as compared to upper extremity: Should be apparent by 5 days of age

 

Oxygen desaturation out of proportion of what would be expected based on physical examination or differential between upper and lower extremity: Less than 95% in both extremities or greater than 4% difference between upper and lower extremity

 

Abnormal femoral pulses: Absent or diminished relative to the brachial pulses

 

Signs of congestive heart failure: Facial edema, hepatomegaly (especially greater than 2.5 cm below costal margin), pulmonary edema

 

Abnormal cardiac examination, especially 1 of the 6 cardinal signs:

Pansystolic murmur

Intensity of the murmur greater than or equal to grade 3

Point of maximal intensity at the upper left sternal border

Harsh quality of murmur

Early mid-systolic click

Abnormal second heart sound

Non-Cardiogenic Etiologies In The Differential Diagnosis Of CHD

Respiratory:

Bronchiolitis

Pneumonia

Spontaneous pneumothorax

Laryngomalacia

Pulmonary hemangioma

Cystic adenomatoid malformation

Reactive airways disease

 

Hemodynamic:

Sepsis

Anaphylaxis

 

Gastrointestinal:

Gastroesophageal reflux

Tracheoesophageal fistula

 

Other:

Non-accidental trauma

 

Toxic/Metabolic:

Methemoglobinemia

Toxic ingestion

Congenital adrenal hyperplasia

Congenital Heart Disease In Children: Key Points

1. Because sepsis is strongly suspected in any neonate presenting to the emergency department in distress, a complete diagnostic evaluation for infection should be performed, and antibiotic therapy should be initiated concomitant with the evaluation for CHD.

2. Despite recent advances in antenatal ultrasound, the majority of patients with CHD are diagnosed after delivery.

3. Functional closure of the DA may be delayed in children with CHD. As a result, patients with ductal-dependent lesions will become symptomatic after discharge from the neonatal nursery.

4. The timing of presentation of CHD is bimodal. Patients with ductal-dependent defects will present in the first month of life, while patients with predominantly left-to-right shunting lesions will present between 2-6 months of age.

5. A ductal-dependent CHD should be considered in any neonate less than 1 month of age who presents with sudden cardiovascular collapse. These lesions have the highest incidence of mortality prior to surgical correction.

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Congenital Heart Disease In Children: Risk Management Pitfalls

1. “If the patient had CHD, the diagnosis would have been made in utero or prior to leaving the newborn nursery.” Recent studies estimate that greater than 60% of CHD cases are not diagnosed on antenatal ultrasound. Most neonates with CHD are clinically asymptomatic immediately after birth. Even when abnormalities such as a murmur are detected on physical examination, many will not be directly referred to a pediatric cardiologist.

2. “The patient is greater than 1 week old, so the diagnosis cannot be a ductal-dependent CHD. The DA should have closed days ago.” Patients with ductal-dependent cardiac disease, especially ductal-dependent systemic blood flow, may have persistence of DA patency beyond 24 hours of life as a result of increased DA blood flow. Cardiovascular collapse in a child less than 1 month of age should be considered as a CHD with ductal-dependent systemic blood flow until proven otherwise.

3. “The infant is febrile. We should evaluate and treat for sepsis. CHD is not likely.” While sepsis is more common and should be suspected in any neonate presenting to the emergency department with tachypnea, cyanosis, or shock, a diagnosis of CHD should not be excluded based solely on the presence of fever. In fact, the presentation of a patient with CHD may be precipitated by an infectious process.

4. “The blood pressure and SpO2 obtained in triage are normal. I’m reassured.” Infants presenting to the emergency room in distress should have blood pressure and SpO2 measurements performed on the right upper extremity and one lower extremity. A discrepancy between the two extremities is suggestive of CHD.

5. “No one can hear a murmur on this infant. Therefore, CHD is not likely.” In many patients with CHD, especially those presenting with marked tachycardia, a murmur will not be present or will be difficult to auscultate. The presence of a murmur should raise suspicions for CHD, but the absence of a murmur does not exclude the diagnosis.

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Congenital Heart Disease In Children: Case Study

Case Study:

It’s January, the middle of “RSV season,” when a 2-week-old infant is brought to the emergency department by his mother because he was “breathing fast all night.” His birth history is unremarkable, and his mother claims that he had been doing well until yesterday breastfeeding, urinating, and stooling regularly. In triage, physical examination is remarkable for an irritable child with a respiratory rate (RR) of 60 breaths per minute, a heart rate (HR) of 170 beats per minute, right upper extremity blood pressure of 70/50 mmHg, axillary temperature of 37°C (99°F), and oxygen saturation as determined by pulse oximetry of 85%. Skin and mucous membranes appear dry. Extremities are cool with a capillary refill time of 4 seconds. Nasal flaring and moderate intercostals retractions are noted, and expiratory wheezing is heard bilaterally. No murmur is noted, and the liver edge is 3 cm below the right costal margin.

Supplemental oxygen is administered by a facemask and SpO2 increases to 90%. The initial concerns are RSV bronchiolitis or sepsis. An inhaled albuterol treatment is started, a capillary blood gas is obtained, intravenous access is promptly accomplished, and he receives two 20 mL/kg fluid boluses with no improvement. In fact, vital signs have deteriorated to RR 60, HR 180, BP 62/38, SpO2 86%, and crackles are auscultated on repeat examination of lungs. Extremities remain cool and mottled, and liver is now 5 cm below costal margin. A chest x-ray shows a normal sized heart, prominent pulmonary vascular markings, and mild bilateral hyperinflation. Arterial blood gas results are reported as follows: pH 7.26, pCO2 20 torr, and pO2 60 torr. At this point, one of the residents asks, “Could this patient have congenital heart disease?”

Conclusion to the above case study…

The patient presented in the opening vignette was ultimately diagnosed with critical aortic stenosis. Presentation to the emergency department occurred following delayed closure of the DA. The abrupt development of symptoms and presence of hepatomegaly provided early clues to the diagnosis, but the patient’s clinical deterioration following treatment with inhaled albuterol and aggressive intravenous fluid boluses increased the likelihood of CHD. The patient was subsequently endotracheally intubated, administered PGE via continuous infusion, and transferred to a tertiary care facility for surgical correction.

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Sepsis Diagnosis

Documented Or Suspected Infection And “Some” Of The Following

 

• Hyperthermia (T > 38.3°C [100.94°F])

• Hypothermia (T < 36°C [96.8°F])

• Tachycardia (HR > 90/minute)

• Tachypnea (respiratory rate > 20/minute)

• Acutely altered mental status

• Hyperglycemia (glucose > 120 mg/dL) in the absence of diabetes

• Significant edema (> 20 mL/kg positive fluid balance in 24 hours)

 

Signs Of Inflammation

• Leukocytosis (WBC > 12,000/mm) or > 10% immature forms

• Leukopenia (WBC < 4000/mm)

• C-reactive protein > 2 standard deviations above normal

• Plasma procalcitonin > 2 standard deviations above normal

 

Hemodynamics

• Hypotension (SBP < 90 mmHg, MAP < 70 mmHg)

• SvO  > 70%

• Cardiac index > 3.5 L/min/m

 

Organ Dysfunction

• Arterial hypoxemia (PaO/FIO2 < 300)

• Acute oliguria (urine output < 0.5 mL/kg/hr for at least 2 hours

• Creatinine increase > 0.5 mg/dL

• Coagulopathy (INR > 1.5 or PTT > 60 seconds)

• Ileus

• Thrombocytopenia (platelet count < 100,000/mm)

• Hyperbilirubinemia (bilirubin > 4 mg/dL)

 

Tissue Perfusion Variables

• Lactate > 2 mmol/L

• Decreased capillary refill or mottling

Sepsis: Risk Management Pitfalls

1. “She wasn’t febrile, so this can’t be sepsis.” Especially in the elderly, but also in patients with immunocompromise and malignancy, the febrile response to infection can be blunted. These patients also have a higher risk of multi-drug resistant pathogens and higher mortality, so they should be carefully handled.

 

2. “He has a history of congestive heart failure, and he presented short of breath and with peripheral edema; he looked pretty bad, so I put him on BiPAP, and I just gave him a little Lasix™. Lab just called me with a BNP of 550 so this is definitely CHF.” It may be CHF, but not necessarily. The role of BNP in the diagnosis of any disease is contextual, and its elevation in sepsis should make physicians wary of its use to guide decisions. CHF is a common comorbidity of patients with sepsis, and a septic patient with a history of CHF could easily present with shortness of breath, chronic edema, and abnormal lung sounds possibly suggesting volume overload. BNP elevations can occur in sepsis acutely, and it is also possible that the patient chronically has an elevated BNP.

 

3. “This guy was really sick, so I just threw in the central line quick.” The Institute of Health 100,000 Lives campaign identified a number of interventions that hospitals could institute to decrease mortality. Among the interventions were adopting a hospital-wide policy on central line placement and encouraging full sterile technique with pre-procedure hand washing, full drape, surgical cap, mask, gown, and gloves in addition to good technique, no matter the time constraints. Both via this campaign and in smaller studies, adopting a policy for better technique for central line placement had a noticeable impact on morbidity and mortality and has become the accepted standard of care.92

 

4. “My nurses just can’t get a central venous pressure, and he had good peripheral access, so I didn’t want to risk a central line. The ICU team can put it in.” Early Goal-Directed Therapy and subsequent studies have demonstrated a survival benefit in patients receiving goal-directed therapy within the first 6 hours. Accurate measurement of CVP and central venous oxygen saturations are critical to demonstrating the success of interventions intended to volume resuscitate and reverse the oxygen delivery derangements seen in sepsis. Put in the line now; do not wait for transfer to the ICU.

 

5. “He came from home, so I treated the pneumonia as community acquired.” The use of antibiotics with coverage of the eventual isolated organism has been shown to decrease mortality, length of ICU stay, and duration of antibiotics. Patients with health-care associated pneumonia (HCAP) have much the same pattern of atypical and potentially multi-drug resistant organisms as hospitalized patients. HCAP includes anyone hospitalized for 2 or more days within the previous 90 days, anyone residing in or recently discharged from a long term care facility, patients who received intravenous antibiotics, chemotherapy, or complicated wound care within the preceding 30 days, and all hemodialysis patients. Just coming from home does not qualify as “community acquired,” and patients who receive their care from multiple institutions and locations may require careful questioning to determine that they need a different cocktail of empiric antibiotics.

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Sepsis: Case Study

Case Study…
As you start your shift, you’re handed the chart of an 82-year-old nursing home patient with urosepsis who is waiting for a bed. Your colleague remarks, “She got some fluids, the antibiotics are in, she looks good, and she’s much more ‘with it’ now. The family says she’s pretty much at baseline mental status now. She’s headed to the floor in a bit.” 

Later in your shift, you see a 43-year-old male with a history of well-controlled diabetes but no other medical history. He presents awake, alert, but ill appearing and short of breath. Over the next few hours he becomes febrile and confused. His respiratory status declines, and he requires intubation. His blood pressure is difficult to support despite aggressive fluid resuscitation and vasopressors. His blood glucose is greater than 600, his blood lactate level was elevated on arrival, and it further increased prior to transfer to the ICU. His creatinine is very elevated and he develops DIC. He requires 1-to-1 nursing with additional help from other staff and a considerable amount of your time, essentially grinding your ED to a halt. Upon moving the patient to the ICU, you report to the admitting intensivist, “This guy is really septic.” In following up on the patient, you discover that he expired after 48 hours in the ICU. 

In reviewing the shift, it occurs to you that the same diagnostic label was applied to a disease process in which an 82-year-old nursing home patient recovered largely in the ED and went to the floor while a reasonably healthy younger person became desperately ill and expired in an ICU. 

Is this really the same disease process? Are there symptoms, signs, or tests that accurately identify patients with infections that are likely to become septic? Are there interventions in the ED that could improve the chance of survival of the young man above?

Conclustion of the above case study…
Returning to our initial cases: The decision to admit a nursing home patient to a medical ward after therapy in the ED was informed by the use of a MEDS score78 and a lactate level64 to determine a low risk of mortality and to identify a patient unlikely to require or benefit from more aggressive interventions and unlikely to need subsequent transfers to the ICU. 

As for the second case, our ability to review pathophysiology and prognostic indicators of poor outcome reveal a patient with increasing rather than improving lactate, altered mental status, DIC, and multi-organ failure. His blood cultures return positive with a Gram-negative organism in less than 24 hours. His chance of survival is very small. The application of a goal-directed therapeutic plan with aggressive volume correction, optimized oxygen delivery, prompt delivery of antibiotics with activity against the responsible organism, support of cardiac output and function, and possibly the addition of specific medications for reversal or moderation of sepsis physiology may result in improvement. This may include a decreasing lactate4 preserved or improving cardiac performance, a normal or near normal glucose, replacement steroids for a dysfunctional adrenal gland, and replacement of depleted blood products, such as oxygen-carrying hemoglobin or even coagulation cascade products like protein C.

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