Pediatric Abdominal Trauma (Dr. Blumberg):
- Number one initially UNrecognized causes of death in pediatrics
- Relatively larger organs compared to body sizes –> increase in injury
- Children can maintain BP even up to 30% blood volume loss so hypotension is a late sign of hemorrhage
- Less likely to scan children 2/2 concern for radiation in children
- PECARN Abdomen variables:
- Evidence of abdominal wall trauma or seat-belt sign
- GCS < 14
- Abdominal tenderness
- Evidence of thoracic wall trauma
- Complaints of abdominal pain
- Decreased breath sounds
- Vomiting
- These 7 variables identified 197 out of the 203 patients with intraabdominal injuries
- Of the 5034 patients deemed very low risk (no prediction variables present), 6 had intraabdominal injuries, requiring interventions
- Data: Sensitivity 97%, Specific 43%, Negative PPV near 100%, Positive PPV 3%, negative LR 0.07
Pediatric SIM Case (Hemolytic Uremic Syndrome):
- Ask parents about bloody diarrhea
- HUS Classification
- Diarrhea (typical) VS no-diarrhea (atypical)
- Primary VS Secondary
- Primary: defects in complement activation system
- Secondary causes: infection (E. Coli, S. PNA, HIV), drug toxicity, autoimmune
- Classic Triad (after prodromal period of diarrhea)
- Microangiopathic hemolytic anemia
- Hb < 8 g/dL
- Peripheral blood smear: large number of schistocytes and helmet cells
- Negative Coomb’s test
- Thrombocytopenia
- Platelets usually ~40,000/mm3
- Acute kidney injury
- Can range from hematuria to proteinuria to elevated BUN/Cr
- Decreased urine output
- Microangiopathic hemolytic anemia
- How can I differentiate HUS from DIC?
- DIC can reveal:
- Prolonged PT and PTT
- Elevated levels of fibrin degradation products and D-Dimer
- DIC can reveal:
- MCC of HUS = Shiga-toxin producing E. Coli (EHEC 0157:H7)
- Management:
- Monitor fluid status carefully
- Usually dehydrated and require bolus (20cc/kg)
- Sometimes, oliguric or anuric patients may be fluid overloaded
- May require dialysis, depending on degree of renal failure and complications
- Transfuse for hemoglobin <6 g/dL for goal of 8-9 g/dL
- Rarely have to transfuse platelets (only if active bleeding or <30,000/mm3 and requiring invasive procedure)
- Monitor for seizures
- Avoid antibiotics (unless sepsis is strongly suspected) because of potential release of Shiga toxin from lysis of bacterial cells
- As discussed by Carlo and Dr. Restivo, final common pathway between HUS and TTP is ADAMTS-13 depletion. Therefore, can consider plasma exchange with FFP to remove the autoantibodies to ADAMTS13 protein and replete it
- Monitor fluid status carefully
- For further reading, check out EMDocs post
Adult SIM Case (Tumor Lysis Syndrome)
- Massive tumor cell breakdown –> release of large amounts of potassium, phosphate and nucleic acids
- Catabolism of nucleic acids to uric acid –> hyperuricemia –> precipitation of uric acid in renal tubules –> AKI
- Hyperphosphatemia with calcium phosphate deposition in renal tubules –> AKI
- Hyperkalemia –> cardiac arrest
- Laboratory Criteria (from UpToDate)
- Uric Acid > 8 mg/dL
- Potassium > 6 mEq/L
- Phosphorous >4.5 mg/dL
- Calcium < 7 mg/dL
- Clinical tumor lysis syndrome = laboratory criteria + at least 1 clinical complication
- Most often occurs after initiation of cytotoxic therapy in aggressive lymphomas and T-cell ALL
- Can also occur spontaneously prior to onset of chemo (especially in non-Hodgkin lymphoma)
- Management:
- Treat electrolyte abnormalities
- Can use Rasburicase at 0.2mg/kg (if not given initially as prophylaxis)
- Fluids (to wash out obstructing uric acid crystals)
- Should be admitted to ICU
- Consider renal consult for possible dialysis
- If initial calcium dose for hyperkalemia is not effective (ex: persistently bradycardia), repeat dose!